TY  - CONF
AU  - Saksida, Tamara
AU  - Mićanović, Dragica
AU  - Koprivica, Ivan
AU  - Nikolić, Ivana
AU  - Vujičić, Milica
AU  - Stošić-Grujičić, Stanislava
AU  - Stojanović, Ivana D.
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5766
AB  - Macrophage migration inhibitory factor (MIF) is a molecule expressed both by the immune
cells, like T, B lymphocytes and macrophages, and non-immune cells, like adipocytes,
hepatocytes and beta cells of pancreatic islets. It has actions in the innate and adaptive
immunity, such as a part in regulating the interleukin-17 expression and production, but also
in the development of chemically induced type 1 diabetes in mice. This paper summarizes our
results on the role of MIF in the development of obesity and type 2 diabetes, done in vitro on
beta cell models and murine pancreatic islets, as well as in vivo, when mice with MIF deletion
(MIF-KO) and their wild type (wt) counterparts were on a high fat diet. It is considered that
obesity can develop as a consequence of altered intestinal permeability, so potential leakage of
the intestinal barrier is investigated in the MIF-KO and wt mice. Also, the interplay between
MIF and regulatory T cells, as an important regulator of inflammation in the adipose tissue, is
explored at the level of visceral adipose tissue.
PB  - Belgrade: Faculty of Chemistry
C3  - Biochemistry of Control in Life and Technology: Serbian Biochemical Society Seventh Conference with International Participation. 2017 Nov 10; Belgrade, Serbia
T1  - The role of macrophage migration inhibitory factor in the development of obesity and altered intestinal permeability
SP  - 101
EP  - 107
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5766
ER  - 

@conference{
author = "Saksida, Tamara and Mićanović, Dragica and Koprivica, Ivan and Nikolić, Ivana and Vujičić, Milica and Stošić-Grujičić, Stanislava and Stojanović, Ivana D.",
year = "2017",
abstract = "Macrophage migration inhibitory factor (MIF) is a molecule expressed both by the immune
cells, like T, B lymphocytes and macrophages, and non-immune cells, like adipocytes,
hepatocytes and beta cells of pancreatic islets. It has actions in the innate and adaptive
immunity, such as a part in regulating the interleukin-17 expression and production, but also
in the development of chemically induced type 1 diabetes in mice. This paper summarizes our
results on the role of MIF in the development of obesity and type 2 diabetes, done in vitro on
beta cell models and murine pancreatic islets, as well as in vivo, when mice with MIF deletion
(MIF-KO) and their wild type (wt) counterparts were on a high fat diet. It is considered that
obesity can develop as a consequence of altered intestinal permeability, so potential leakage of
the intestinal barrier is investigated in the MIF-KO and wt mice. Also, the interplay between
MIF and regulatory T cells, as an important regulator of inflammation in the adipose tissue, is
explored at the level of visceral adipose tissue.",
publisher = "Belgrade: Faculty of Chemistry",
journal = "Biochemistry of Control in Life and Technology: Serbian Biochemical Society Seventh Conference with International Participation. 2017 Nov 10; Belgrade, Serbia",
title = "The role of macrophage migration inhibitory factor in the development of obesity and altered intestinal permeability",
pages = "101-107",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5766"
}

Saksida, T., Mićanović, D., Koprivica, I., Nikolić, I., Vujičić, M., Stošić-Grujičić, S.,& Stojanović, I. D.. (2017). The role of macrophage migration inhibitory factor in the development of obesity and altered intestinal permeability. in Biochemistry of Control in Life and Technology: Serbian Biochemical Society Seventh Conference with International Participation. 2017 Nov 10; Belgrade, Serbia
Belgrade: Faculty of Chemistry., 101-107.
https://hdl.handle.net/21.15107/rcub_ibiss_5766

Saksida T, Mićanović D, Koprivica I, Nikolić I, Vujičić M, Stošić-Grujičić S, Stojanović ID. The role of macrophage migration inhibitory factor in the development of obesity and altered intestinal permeability. in Biochemistry of Control in Life and Technology: Serbian Biochemical Society Seventh Conference with International Participation. 2017 Nov 10; Belgrade, Serbia. 2017;:101-107.
https://hdl.handle.net/21.15107/rcub_ibiss_5766 .

Saksida, Tamara, Mićanović, Dragica, Koprivica, Ivan, Nikolić, Ivana, Vujičić, Milica, Stošić-Grujičić, Stanislava, Stojanović, Ivana D., "The role of macrophage migration inhibitory factor in the development of obesity and altered intestinal permeability" in Biochemistry of Control in Life and Technology: Serbian Biochemical Society Seventh Conference with International Participation. 2017 Nov 10; Belgrade, Serbia (2017):101-107,
https://hdl.handle.net/21.15107/rcub_ibiss_5766 .

TY  - JOUR
AU  - Nikolić, Ivana
AU  - Stojanović, Ivana D.
AU  - Vujičić, Milica
AU  - Fagone, Paolo
AU  - Mangano, Katia
AU  - Stošić-Grujičić, Stanislava
AU  - Nicoletti, Ferdinando
AU  - Saksida, Tamara
PY  - 2017
UR  - http://linkinghub.elsevier.com/retrieve/pii/S0171298516303746
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2484
AB  - Bovine colostrum is a rich source of nutrients and immunologically active components that play a role in conveying passive immunity to the offspring, protection and maturation of new-born's gastrointestinal tract. Colostrum has exerted positive effects in diseases affecting gastrointestinal tract, as well as type 2 diabetes (T2D). However, health-promoting effects in type 1 diabetes have not been reported. The aim of this study was to investigate therapeutic value of oral administration of standardized bovine colostrum derivative (SBCD) in three models of type 1 diabetes (T1D): spontaneously developed T1D in NOD mice and BB-DP rats, and in chemically induced T1D in C57BL/6 mice with multiple low doses of streptozotocin (MLDS). SBCD was administered per os and the disease development was evaluated by weekly measurement of blood glucose and by histological analyses of the pancreas. SBCD administration prevented diabetes development in all three models, as indicated by euglicaemia. Ex vivo analysis of cytokine expression and production in the spleen and mesenteric lymph nodes (MLN) in MLDS challenged mice revealed a strong modulation of the immune response. In the MLN cells SBCD disrupted harmful Th17 response induced by MLDS. Expression of Th1 signature cytokine IFN-γ was down-regulated in MLN cells of SBCD-treated mice, while IL-4 secretion (Th2 cytokine) was up-regulated in comparison to diabetic group. Modulation of the immune response seen in the MLN protruded to the spleen, giving overall less infiltration of immune cells to the pancreas. SBCD acted on immune cells and halted (auto) aggression towards pancreatic beta cells. Moreover, SBCD induced beta cell proliferation. Hence, this derivative could be tested in diabetes and other similar diseases with aberrant immune response.
T2  - Immunobiology
T1  - Standardized bovine colostrum derivative impedes development of type 1 diabetes in rodents
IS  - 2
VL  - 222
DO  - 10.1016/j.imbio.2016.09.013
SP  - 272
EP  - 279
ER  - 

@article{
author = "Nikolić, Ivana and Stojanović, Ivana D. and Vujičić, Milica and Fagone, Paolo and Mangano, Katia and Stošić-Grujičić, Stanislava and Nicoletti, Ferdinando and Saksida, Tamara",
year = "2017",
abstract = "Bovine colostrum is a rich source of nutrients and immunologically active components that play a role in conveying passive immunity to the offspring, protection and maturation of new-born's gastrointestinal tract. Colostrum has exerted positive effects in diseases affecting gastrointestinal tract, as well as type 2 diabetes (T2D). However, health-promoting effects in type 1 diabetes have not been reported. The aim of this study was to investigate therapeutic value of oral administration of standardized bovine colostrum derivative (SBCD) in three models of type 1 diabetes (T1D): spontaneously developed T1D in NOD mice and BB-DP rats, and in chemically induced T1D in C57BL/6 mice with multiple low doses of streptozotocin (MLDS). SBCD was administered per os and the disease development was evaluated by weekly measurement of blood glucose and by histological analyses of the pancreas. SBCD administration prevented diabetes development in all three models, as indicated by euglicaemia. Ex vivo analysis of cytokine expression and production in the spleen and mesenteric lymph nodes (MLN) in MLDS challenged mice revealed a strong modulation of the immune response. In the MLN cells SBCD disrupted harmful Th17 response induced by MLDS. Expression of Th1 signature cytokine IFN-γ was down-regulated in MLN cells of SBCD-treated mice, while IL-4 secretion (Th2 cytokine) was up-regulated in comparison to diabetic group. Modulation of the immune response seen in the MLN protruded to the spleen, giving overall less infiltration of immune cells to the pancreas. SBCD acted on immune cells and halted (auto) aggression towards pancreatic beta cells. Moreover, SBCD induced beta cell proliferation. Hence, this derivative could be tested in diabetes and other similar diseases with aberrant immune response.",
journal = "Immunobiology",
title = "Standardized bovine colostrum derivative impedes development of type 1 diabetes in rodents",
number = "2",
volume = "222",
doi = "10.1016/j.imbio.2016.09.013",
pages = "272-279"
}

Nikolić, I., Stojanović, I. D., Vujičić, M., Fagone, P., Mangano, K., Stošić-Grujičić, S., Nicoletti, F.,& Saksida, T.. (2017). Standardized bovine colostrum derivative impedes development of type 1 diabetes in rodents. in Immunobiology, 222(2), 272-279.
https://doi.org/10.1016/j.imbio.2016.09.013

Nikolić I, Stojanović ID, Vujičić M, Fagone P, Mangano K, Stošić-Grujičić S, Nicoletti F, Saksida T. Standardized bovine colostrum derivative impedes development of type 1 diabetes in rodents. in Immunobiology. 2017;222(2):272-279.
doi:10.1016/j.imbio.2016.09.013 .

Nikolić, Ivana, Stojanović, Ivana D., Vujičić, Milica, Fagone, Paolo, Mangano, Katia, Stošić-Grujičić, Stanislava, Nicoletti, Ferdinando, Saksida, Tamara, "Standardized bovine colostrum derivative impedes development of type 1 diabetes in rodents" in Immunobiology, 222, no. 2 (2017):272-279,
https://doi.org/10.1016/j.imbio.2016.09.013 . .

TY  - JOUR
AU  - Vujičić, Milica
AU  - Vasić, Bobana
AU  - Nikolić, Ivana
AU  - Saksida, Tamara
AU  - Stojanović, Ivana D.
PY  - 2017
UR  - http://www.doiserbia.nb.rs/Article.aspx?ID=0354-46641600096V
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2978
UR  - http://www.serbiosoc.org.rs/arch/index.php/abs/article/view/812
AB  - Nuclear protein 1 (NUPR1) is a transcription cofactor that senses stressful conditions and modulates cellular response by promoting or inhibiting apoptosis. NUPR1 is usually highly expressed in tumor cells where it enables them to adapt and resist environmental stress or chemotherapeutic compounds. NUPR1 can be involved in cell proliferation. Data about the involvement of NUPR1 in the proliferation and apoptosis of lymphocytes are scarce. Therefore, in this study we focused on the role of NUPR1 in lymphocyte physiology and found that NUPR1 might be involved in the initiation of their proliferation. Lymphocytes were isolated from the cervical lymph nodes of C57BL/6 mice. NUPR1 expression subsided 24 h after the induction of proliferation by a mitogen. Also, stressful conditions after cell isolation led to increased NUPR1 mRNA and protein expression in vitro that coincided with cell apoptosis. Similarly, apoptosis induction by staurosporine, a broad-range protein kinase inhibitor, led to increased NUPR1 expression. In addition, NUPR1 inhibition by smallinterfering RNA prevented the staurosporine-induced apoptosis (judging from decreased caspase activity) in the whole cell population of cervical lymph nodes. However, NUPR1 absence was irrelevant to the induction of apoptosis in CD3+ T lymphocytes, suggesting that NUPR1 is probably a mediator of apoptosis in other immune cell populations within the lymph node, such as B lymphocytes. In conclusion, our results suggest that NUPR1 is important for the initiation of lymphocyte cell division and for the apoptotic process of non-T cells during stressful conditions.
T2  - Archives of Biological Sciences
T1  - The role of NUPR1 in lymphocyte proliferation and apoptosis
IS  - 2
VL  - 69
DO  - 10.2298/ABS160707096V
SP  - 261
EP  - 267
ER  - 

@article{
author = "Vujičić, Milica and Vasić, Bobana and Nikolić, Ivana and Saksida, Tamara and Stojanović, Ivana D.",
year = "2017",
abstract = "Nuclear protein 1 (NUPR1) is a transcription cofactor that senses stressful conditions and modulates cellular response by promoting or inhibiting apoptosis. NUPR1 is usually highly expressed in tumor cells where it enables them to adapt and resist environmental stress or chemotherapeutic compounds. NUPR1 can be involved in cell proliferation. Data about the involvement of NUPR1 in the proliferation and apoptosis of lymphocytes are scarce. Therefore, in this study we focused on the role of NUPR1 in lymphocyte physiology and found that NUPR1 might be involved in the initiation of their proliferation. Lymphocytes were isolated from the cervical lymph nodes of C57BL/6 mice. NUPR1 expression subsided 24 h after the induction of proliferation by a mitogen. Also, stressful conditions after cell isolation led to increased NUPR1 mRNA and protein expression in vitro that coincided with cell apoptosis. Similarly, apoptosis induction by staurosporine, a broad-range protein kinase inhibitor, led to increased NUPR1 expression. In addition, NUPR1 inhibition by smallinterfering RNA prevented the staurosporine-induced apoptosis (judging from decreased caspase activity) in the whole cell population of cervical lymph nodes. However, NUPR1 absence was irrelevant to the induction of apoptosis in CD3+ T lymphocytes, suggesting that NUPR1 is probably a mediator of apoptosis in other immune cell populations within the lymph node, such as B lymphocytes. In conclusion, our results suggest that NUPR1 is important for the initiation of lymphocyte cell division and for the apoptotic process of non-T cells during stressful conditions.",
journal = "Archives of Biological Sciences",
title = "The role of NUPR1 in lymphocyte proliferation and apoptosis",
number = "2",
volume = "69",
doi = "10.2298/ABS160707096V",
pages = "261-267"
}

Vujičić, M., Vasić, B., Nikolić, I., Saksida, T.,& Stojanović, I. D.. (2017). The role of NUPR1 in lymphocyte proliferation and apoptosis. in Archives of Biological Sciences, 69(2), 261-267.
https://doi.org/10.2298/ABS160707096V

Vujičić M, Vasić B, Nikolić I, Saksida T, Stojanović ID. The role of NUPR1 in lymphocyte proliferation and apoptosis. in Archives of Biological Sciences. 2017;69(2):261-267.
doi:10.2298/ABS160707096V .

Vujičić, Milica, Vasić, Bobana, Nikolić, Ivana, Saksida, Tamara, Stojanović, Ivana D., "The role of NUPR1 in lymphocyte proliferation and apoptosis" in Archives of Biological Sciences, 69, no. 2 (2017):261-267,
https://doi.org/10.2298/ABS160707096V . .

TY  - JOUR
AU  - Vujičić, Milica
AU  - Vasić, Bobana
AU  - Nikolić, Ivana
AU  - Saksida, Tamara
AU  - Stojanović, Ivana D.
PY  - 2016
UR  - http://www.doiserbia.nb.rs/Article.aspx?ID=0354-46641600096V
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2690
AB  - Nuclear protein 1 (NUPR1) is a transcription cofactor that senses stressful conditions and modulates cellular response by promoting or inhibiting apoptosis. NUPR1 is usually highly expressed in tumor cells where it enables them to adapt and resist environmental stress or chemotherapeutic compounds. NUPR1 can be involved in cell proliferation. Data about the involvement of NUPR1 in the proliferation and apoptosis of lymphocytes are scarce. Therefore, in this study we focused on the role of NUPR1 in lymphocyte physiology and found that NUPR1 might be involved in the initiation of their proliferation. Lymphocytes were isolated from the cervical lymph nodes of C57BL/6 mice. NUPR1 expression subsided 24 h after the induction of proliferation by a mitogen. Also, stressful conditions after cell isolation led to increased NUPR1 mRNA and protein expression in vitro that coincided with cell apoptosis. Similarly, apoptosis induction by staurosporine, a broad-range protein kinase inhibitor, led to increased NUPR1 expression. In addition, NUPR1 inhibition by smallinterfering RNA prevented the staurosporine-induced apoptosis (judging from decreased caspase activity) in the whole cell population of cervical lymph nodes. However, NUPR1 absence was irrelevant to the induction of apoptosis in CD3+ T lymphocytes, suggesting that NUPR1 is probably a mediator of apoptosis in other immune cell populations within the lymph node, such as B lymphocytes. In conclusion, our results suggest that NUPR1 is important for the initiation of lymphocyte cell division and for the apoptotic process of non-T cells during stressful conditions.
T2  - Archives of Biological Sciences
T1  - The role of NUPR1 in lymphocyte proliferation and apoptosis
DO  - 10.2298/ABS160707096V
ER  - 

@article{
author = "Vujičić, Milica and Vasić, Bobana and Nikolić, Ivana and Saksida, Tamara and Stojanović, Ivana D.",
year = "2016",
abstract = "Nuclear protein 1 (NUPR1) is a transcription cofactor that senses stressful conditions and modulates cellular response by promoting or inhibiting apoptosis. NUPR1 is usually highly expressed in tumor cells where it enables them to adapt and resist environmental stress or chemotherapeutic compounds. NUPR1 can be involved in cell proliferation. Data about the involvement of NUPR1 in the proliferation and apoptosis of lymphocytes are scarce. Therefore, in this study we focused on the role of NUPR1 in lymphocyte physiology and found that NUPR1 might be involved in the initiation of their proliferation. Lymphocytes were isolated from the cervical lymph nodes of C57BL/6 mice. NUPR1 expression subsided 24 h after the induction of proliferation by a mitogen. Also, stressful conditions after cell isolation led to increased NUPR1 mRNA and protein expression in vitro that coincided with cell apoptosis. Similarly, apoptosis induction by staurosporine, a broad-range protein kinase inhibitor, led to increased NUPR1 expression. In addition, NUPR1 inhibition by smallinterfering RNA prevented the staurosporine-induced apoptosis (judging from decreased caspase activity) in the whole cell population of cervical lymph nodes. However, NUPR1 absence was irrelevant to the induction of apoptosis in CD3+ T lymphocytes, suggesting that NUPR1 is probably a mediator of apoptosis in other immune cell populations within the lymph node, such as B lymphocytes. In conclusion, our results suggest that NUPR1 is important for the initiation of lymphocyte cell division and for the apoptotic process of non-T cells during stressful conditions.",
journal = "Archives of Biological Sciences",
title = "The role of NUPR1 in lymphocyte proliferation and apoptosis",
doi = "10.2298/ABS160707096V"
}

Vujičić, M., Vasić, B., Nikolić, I., Saksida, T.,& Stojanović, I. D.. (2016). The role of NUPR1 in lymphocyte proliferation and apoptosis. in Archives of Biological Sciences.
https://doi.org/10.2298/ABS160707096V

Vujičić M, Vasić B, Nikolić I, Saksida T, Stojanović ID. The role of NUPR1 in lymphocyte proliferation and apoptosis. in Archives of Biological Sciences. 2016;.
doi:10.2298/ABS160707096V .

Vujičić, Milica, Vasić, Bobana, Nikolić, Ivana, Saksida, Tamara, Stojanović, Ivana D., "The role of NUPR1 in lymphocyte proliferation and apoptosis" in Archives of Biological Sciences (2016),
https://doi.org/10.2298/ABS160707096V . .

TY  - JOUR
AU  - Vujičić, Milica
AU  - Nikolić, Ivana
AU  - Kontogianni, Vassiliki G.
AU  - Saksida, Tamara
AU  - Charisiadis, Pantelis
AU  - Vasić, Bobana
AU  - Stošić-Grujičić, Stanislava
AU  - Gerothanassis, Ioannis P.
AU  - Tzakos, Andreas G.
AU  - Stojanović, Ivana D.
PY  - 2016
UR  - http://doi.wiley.com/10.1111/1750-3841.13333
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2979
AB  - Type 1 diabetes (T1D) is an autoimmune disease that develops as a consequence of pancreatic β-cell death induced by proinflammatory mediators. Because Origanum vulgare L. ssp. hirtum (Greek oregano) contains antiinflammatory molecules, we hypothesized that it might be beneficial for the treatment of T1D. An ethyl acetate extract of oregano (EAO) was prepared from the leaves by a polar extraction method. Phytochemical composition was determined by liquid chromatography-UV diode array coupled to ion-trap mass spectrometry with electrospray ionization interface (LC/DAD/ESI-MSn). In vitro immunomodulatory effect of EAO was estimated by measuring proliferation (MTT) or cytokine secretion (ELISA) from immune cells. Diabetes was induced by multiple low doses of streptozotocin (MLDS) in male C57BL/6 mice and EAO was administered intraperitoneally for 10 d. Determination of cellular composition (flow cytometry) and cytokine production (ELISA) was performed on 12th d after diabetes induction. EAO suppressed the function of both macrophages and lymphocytes in vitro. In vivo, EAO treatment significantly preserved pancreatic islets and reduced diabetes incidence in MLDS-challenged mice. Besides down-modulatory effect on macrophages, EAO reduced the number of total CD4+ and activated CD4+CD25+ T cells. Furthermore, EAO affected the number of T helper 1 (Th1) and T helper 17 (Th17) cells through downregulation of their key transcription factors T-bet and RORγT. Because EAO treatment protects mice from development of hyperglycemia by reducing proinflammatory macrophage/Th1/Th17 response, this plant extract could represent a basis for future diabetes therapy.
PB  - Blackwell Publishing Inc.
T2  - Journal of Food Science
T1  - Ethyl Acetate Extract of Origanum vulgare L. ssp. hirtum Prevents Streptozotocin-Induced Diabetes in C57BL/6 Mice
IS  - 7
VL  - 81
DO  - 10.1111/1750-3841.13333
SP  - H1846
EP  - H1853
ER  - 

@article{
author = "Vujičić, Milica and Nikolić, Ivana and Kontogianni, Vassiliki G. and Saksida, Tamara and Charisiadis, Pantelis and Vasić, Bobana and Stošić-Grujičić, Stanislava and Gerothanassis, Ioannis P. and Tzakos, Andreas G. and Stojanović, Ivana D.",
year = "2016",
abstract = "Type 1 diabetes (T1D) is an autoimmune disease that develops as a consequence of pancreatic β-cell death induced by proinflammatory mediators. Because Origanum vulgare L. ssp. hirtum (Greek oregano) contains antiinflammatory molecules, we hypothesized that it might be beneficial for the treatment of T1D. An ethyl acetate extract of oregano (EAO) was prepared from the leaves by a polar extraction method. Phytochemical composition was determined by liquid chromatography-UV diode array coupled to ion-trap mass spectrometry with electrospray ionization interface (LC/DAD/ESI-MSn). In vitro immunomodulatory effect of EAO was estimated by measuring proliferation (MTT) or cytokine secretion (ELISA) from immune cells. Diabetes was induced by multiple low doses of streptozotocin (MLDS) in male C57BL/6 mice and EAO was administered intraperitoneally for 10 d. Determination of cellular composition (flow cytometry) and cytokine production (ELISA) was performed on 12th d after diabetes induction. EAO suppressed the function of both macrophages and lymphocytes in vitro. In vivo, EAO treatment significantly preserved pancreatic islets and reduced diabetes incidence in MLDS-challenged mice. Besides down-modulatory effect on macrophages, EAO reduced the number of total CD4+ and activated CD4+CD25+ T cells. Furthermore, EAO affected the number of T helper 1 (Th1) and T helper 17 (Th17) cells through downregulation of their key transcription factors T-bet and RORγT. Because EAO treatment protects mice from development of hyperglycemia by reducing proinflammatory macrophage/Th1/Th17 response, this plant extract could represent a basis for future diabetes therapy.",
publisher = "Blackwell Publishing Inc.",
journal = "Journal of Food Science",
title = "Ethyl Acetate Extract of Origanum vulgare L. ssp. hirtum Prevents Streptozotocin-Induced Diabetes in C57BL/6 Mice",
number = "7",
volume = "81",
doi = "10.1111/1750-3841.13333",
pages = "H1846-H1853"
}

Vujičić, M., Nikolić, I., Kontogianni, V. G., Saksida, T., Charisiadis, P., Vasić, B., Stošić-Grujičić, S., Gerothanassis, I. P., Tzakos, A. G.,& Stojanović, I. D.. (2016). Ethyl Acetate Extract of Origanum vulgare L. ssp. hirtum Prevents Streptozotocin-Induced Diabetes in C57BL/6 Mice. in Journal of Food Science
Blackwell Publishing Inc.., 81(7), H1846-H1853.
https://doi.org/10.1111/1750-3841.13333

Vujičić M, Nikolić I, Kontogianni VG, Saksida T, Charisiadis P, Vasić B, Stošić-Grujičić S, Gerothanassis IP, Tzakos AG, Stojanović ID. Ethyl Acetate Extract of Origanum vulgare L. ssp. hirtum Prevents Streptozotocin-Induced Diabetes in C57BL/6 Mice. in Journal of Food Science. 2016;81(7):H1846-H1853.
doi:10.1111/1750-3841.13333 .

Vujičić, Milica, Nikolić, Ivana, Kontogianni, Vassiliki G., Saksida, Tamara, Charisiadis, Pantelis, Vasić, Bobana, Stošić-Grujičić, Stanislava, Gerothanassis, Ioannis P., Tzakos, Andreas G., Stojanović, Ivana D., "Ethyl Acetate Extract of Origanum vulgare L. ssp. hirtum Prevents Streptozotocin-Induced Diabetes in C57BL/6 Mice" in Journal of Food Science, 81, no. 7 (2016):H1846-H1853,
https://doi.org/10.1111/1750-3841.13333 . .

TY  - JOUR
AU  - Nikolić, Ivana
AU  - Saksida, Tamara
AU  - Vujičić, Milica
AU  - Stojanović, Ivana D.
AU  - Stošić-Grujičić, Stanislava
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1962
AB  - We have recently shown that carbon monoxide releasing molecule (CORM)-A1
   prevents type 1 diabetes induced in C57BL/6 mice with multiple low doses
   of streptozotocin (MLDS) by shifting the Th1/Th17/M1 balance towards a
   Th2/M2 response. In the present work we tested the hypothesis that
   CORM-A1 might influence regulatory arm of the immune response, as well
   as beta cell regeneration. CORM-A1 (2 mg/kg/day) was administered for 10
   days to mice induced with MLDS and/or depleted of low dose
   cyclophosphamide (CY)-sensitive FoxP3(+) T regulatory (Treg) cells.
   Besides monitoring hyperglycaemia, ex vivo analysis of spleen,
   pancreatic lymph nodes (PLN) and pancreas was performed at the end of
   treatment. In CORM-A1-treated MLDS-induced mice the improvement of
   hyperglycaemia was observed only without depletion of CY-sensitive
   FoxP3(+) Treg cells. This was accompanied by decreased levels of
   interleukin (IL)-12, IL-2 and early activation marker CD25 in the spleen
   and PLN and increased transforming growth factor (TGF)-beta, resulting
   in reduced lymphocyte proliferation in both organs. In parallel,
   decreased transcript levels of IL-2, but increased mRNA expression of
   TGF-beta, accompanied with up-regulation of Ki-67 protein expression was
   observed within pancreas. Together, the data suggested that besides the
   immunomodulatory potential, CORM-A1 probably induces beta cell
   regeneration. (C) 2015 European Federation of Immunological Societies.
   Published by Elsevier B.V. All rights reserved.
T2  - Immunology Letters
T1  - Anti-diabetic actions of carbon monoxide-releasing molecule (CORM)-A1:
 Immunomodulation and regeneration of islet beta cells
IS  - 1
VL  - 165
DO  - 10.1016/j.imlet.2015.03.009
SP  - 39
EP  - 46
ER  - 

@article{
author = "Nikolić, Ivana and Saksida, Tamara and Vujičić, Milica and Stojanović, Ivana D. and Stošić-Grujičić, Stanislava",
year = "2015",
abstract = "We have recently shown that carbon monoxide releasing molecule (CORM)-A1
   prevents type 1 diabetes induced in C57BL/6 mice with multiple low doses
   of streptozotocin (MLDS) by shifting the Th1/Th17/M1 balance towards a
   Th2/M2 response. In the present work we tested the hypothesis that
   CORM-A1 might influence regulatory arm of the immune response, as well
   as beta cell regeneration. CORM-A1 (2 mg/kg/day) was administered for 10
   days to mice induced with MLDS and/or depleted of low dose
   cyclophosphamide (CY)-sensitive FoxP3(+) T regulatory (Treg) cells.
   Besides monitoring hyperglycaemia, ex vivo analysis of spleen,
   pancreatic lymph nodes (PLN) and pancreas was performed at the end of
   treatment. In CORM-A1-treated MLDS-induced mice the improvement of
   hyperglycaemia was observed only without depletion of CY-sensitive
   FoxP3(+) Treg cells. This was accompanied by decreased levels of
   interleukin (IL)-12, IL-2 and early activation marker CD25 in the spleen
   and PLN and increased transforming growth factor (TGF)-beta, resulting
   in reduced lymphocyte proliferation in both organs. In parallel,
   decreased transcript levels of IL-2, but increased mRNA expression of
   TGF-beta, accompanied with up-regulation of Ki-67 protein expression was
   observed within pancreas. Together, the data suggested that besides the
   immunomodulatory potential, CORM-A1 probably induces beta cell
   regeneration. (C) 2015 European Federation of Immunological Societies.
   Published by Elsevier B.V. All rights reserved.",
journal = "Immunology Letters",
title = "Anti-diabetic actions of carbon monoxide-releasing molecule (CORM)-A1:
 Immunomodulation and regeneration of islet beta cells",
number = "1",
volume = "165",
doi = "10.1016/j.imlet.2015.03.009",
pages = "39-46"
}

Nikolić, I., Saksida, T., Vujičić, M., Stojanović, I. D.,& Stošić-Grujičić, S.. (2015). Anti-diabetic actions of carbon monoxide-releasing molecule (CORM)-A1:
 Immunomodulation and regeneration of islet beta cells. in Immunology Letters, 165(1), 39-46.
https://doi.org/10.1016/j.imlet.2015.03.009

Nikolić I, Saksida T, Vujičić M, Stojanović ID, Stošić-Grujičić S. Anti-diabetic actions of carbon monoxide-releasing molecule (CORM)-A1:
 Immunomodulation and regeneration of islet beta cells. in Immunology Letters. 2015;165(1):39-46.
doi:10.1016/j.imlet.2015.03.009 .

Nikolić, Ivana, Saksida, Tamara, Vujičić, Milica, Stojanović, Ivana D., Stošić-Grujičić, Stanislava, "Anti-diabetic actions of carbon monoxide-releasing molecule (CORM)-A1:
 Immunomodulation and regeneration of islet beta cells" in Immunology Letters, 165, no. 1 (2015):39-46,
https://doi.org/10.1016/j.imlet.2015.03.009 . .

TY  - JOUR
AU  - Vujičić, Milica
AU  - Saksida, Tamara
AU  - Nikolić, Ivana
AU  - Stojanović, Ivana D.
AU  - Stošić-Grujičić, Stanislava
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2030
AB  - Compound A (CpdA), or
   2-(4-acetoxyphenyl)-2-chloro-N-methyl-ethyl-ammonium chloride, is a
   stable analog of the hydroxyl phenyl aziridine precursor found in the
   Namibian shrub Salsola tuberculatiformis Botschantzev. It belongs to the
   group of so-called ``dissociated{''} GC receptor ligands that
   downmodulate pro-inflammatory gene expression via the transrepression
   mechanism, but without physically binding to DNA. We have recently
   reported that the in vivo administration of CpdA exerts a strong
   protective effect in a pharmacological model of type 1 diabetes in mice.
   The goal of this study was to investigate in more detail the effects of
   CpdA on multiple immune system components, as well as on target
   pancreatic beta cells in direct in vitro exposure. The utility of CpdA
   in diabetes prevention was evaluated through its addition to
   mitogen-activated spleen, lymph node and peritoneal cells of C57BL/6
   mice, and to murine pancreatic islets and INS-1 and RINm5F beta cell
   lines. CpdA modulated immune cell-derived cytokine production in vitro
   by restraining the pro-inflammatory M1/Th1/Th17 response and switching
   it towards an anti-inflammatory Th2 profile. However, it did not
   preserve beta cells from the cytotoxic action of inflammatory cytokines.
   Thus, the anti-diabetic properties of CpdA are mediated through the
   modulation of immune cell differentiation pathways rather than through
   rescue of target cells from autoimmune attack.
T2  - Archives of Biological Sciences
T1  - In vitro dissection of anti-diabetic effects of compound a, a dissociating glucocorticoid receptor ligand
IS  - 3
VL  - 67
DO  - 10.2298/ABS141107056V
SP  - 941
EP  - 947
ER  - 

@article{
author = "Vujičić, Milica and Saksida, Tamara and Nikolić, Ivana and Stojanović, Ivana D. and Stošić-Grujičić, Stanislava",
year = "2015",
abstract = "Compound A (CpdA), or
   2-(4-acetoxyphenyl)-2-chloro-N-methyl-ethyl-ammonium chloride, is a
   stable analog of the hydroxyl phenyl aziridine precursor found in the
   Namibian shrub Salsola tuberculatiformis Botschantzev. It belongs to the
   group of so-called ``dissociated{''} GC receptor ligands that
   downmodulate pro-inflammatory gene expression via the transrepression
   mechanism, but without physically binding to DNA. We have recently
   reported that the in vivo administration of CpdA exerts a strong
   protective effect in a pharmacological model of type 1 diabetes in mice.
   The goal of this study was to investigate in more detail the effects of
   CpdA on multiple immune system components, as well as on target
   pancreatic beta cells in direct in vitro exposure. The utility of CpdA
   in diabetes prevention was evaluated through its addition to
   mitogen-activated spleen, lymph node and peritoneal cells of C57BL/6
   mice, and to murine pancreatic islets and INS-1 and RINm5F beta cell
   lines. CpdA modulated immune cell-derived cytokine production in vitro
   by restraining the pro-inflammatory M1/Th1/Th17 response and switching
   it towards an anti-inflammatory Th2 profile. However, it did not
   preserve beta cells from the cytotoxic action of inflammatory cytokines.
   Thus, the anti-diabetic properties of CpdA are mediated through the
   modulation of immune cell differentiation pathways rather than through
   rescue of target cells from autoimmune attack.",
journal = "Archives of Biological Sciences",
title = "In vitro dissection of anti-diabetic effects of compound a, a dissociating glucocorticoid receptor ligand",
number = "3",
volume = "67",
doi = "10.2298/ABS141107056V",
pages = "941-947"
}

Vujičić, M., Saksida, T., Nikolić, I., Stojanović, I. D.,& Stošić-Grujičić, S.. (2015). In vitro dissection of anti-diabetic effects of compound a, a dissociating glucocorticoid receptor ligand. in Archives of Biological Sciences, 67(3), 941-947.
https://doi.org/10.2298/ABS141107056V

Vujičić M, Saksida T, Nikolić I, Stojanović ID, Stošić-Grujičić S. In vitro dissection of anti-diabetic effects of compound a, a dissociating glucocorticoid receptor ligand. in Archives of Biological Sciences. 2015;67(3):941-947.
doi:10.2298/ABS141107056V .

Vujičić, Milica, Saksida, Tamara, Nikolić, Ivana, Stojanović, Ivana D., Stošić-Grujičić, Stanislava, "In vitro dissection of anti-diabetic effects of compound a, a dissociating glucocorticoid receptor ligand" in Archives of Biological Sciences, 67, no. 3 (2015):941-947,
https://doi.org/10.2298/ABS141107056V . .

TY  - JOUR
AU  - Vujičić, Milica
AU  - Nikolić, Ivana
AU  - Kontogianni, Vassiliki G.
AU  - Saksida, Tamara
AU  - Charisiadis, Pantelis
AU  - Oreščanin Dušić, Zorana
AU  - Blagojević, Duško
AU  - Stošić-Grujičić, Stanislava
AU  - Tzakos, Andreas G.
AU  - Stojanović, Ivana D.
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1988
AB  - Type 1 diabetes (T1D), an autoimmune inflammatory disorder, develops as
   a consequence of pancreatic beta-cell destruction and results in
   hyperglycaemia. Since current T1D therapy mainly involves insulin
   replacement, the aim of the present study was to evaluate the
   therapeutic potential of Origanum vulgare L. ssp. hirtum (Greek oregano)
   leaf extract rich in biophenols for the treatment of T1D. The
   phytochemical profile of methanolic oregano extract (MOE) and aqueous
   oregano extract (AOE) was determined by liquid
   chromatography/electrospray ion-trap tandem MS (LC/DAD/ESI-MSn), while
   their main compounds were quantified by HPLC with diode array detection.
   After establishing their potent in vitro antioxidant activity, the
   extracts were administered to C57BL/6 mice treated with multiple low
   doses of streptozotocin for diabetes induction. While prophylactic AOE
   therapy had no impact on diabetes induction, MOE reduced diabetes
   incidence and preserved normal insulin secretion. In addition, MOE
   scavenged reactive oxygen and nitrogen species and, therefore,
   alleviated the need for the up-regulation of antioxidant enzymes. MOE
   treatment specifically attenuated the pro-inflammatory response mediated
   by T helper 17 cells and enhanced anti-inflammatory T helper 2 and T
   regulatory cells through the impact on specific signalling pathways and
   transcription factors. Importantly, MOE preserved beta-cells from in
   vitro apoptosis via blockade of caspase 3. Finally, rosmarinic acid, a
   predominant compound in MOE, exhibited only partial protection from
   diabetes induction. In conclusion, acting as an antioxidant,
   immunomodulator and in an anti-apoptotic manner, MOE protected mice from
   diabetes development. Seemingly, there is more than one compound
   responsible for the beneficial effect of MOE.
T2  - British Journal of Nutrition
T1  - Methanolic extract of Origanum vulgare ameliorates type 1 diabetes
 through antioxidant, anti-inflammatory and anti-apoptotic activity
IS  - 5
VL  - 113
DO  - 10.1017/S0007114514004048
SP  - 770
EP  - 782
ER  - 

@article{
author = "Vujičić, Milica and Nikolić, Ivana and Kontogianni, Vassiliki G. and Saksida, Tamara and Charisiadis, Pantelis and Oreščanin Dušić, Zorana and Blagojević, Duško and Stošić-Grujičić, Stanislava and Tzakos, Andreas G. and Stojanović, Ivana D.",
year = "2015",
abstract = "Type 1 diabetes (T1D), an autoimmune inflammatory disorder, develops as
   a consequence of pancreatic beta-cell destruction and results in
   hyperglycaemia. Since current T1D therapy mainly involves insulin
   replacement, the aim of the present study was to evaluate the
   therapeutic potential of Origanum vulgare L. ssp. hirtum (Greek oregano)
   leaf extract rich in biophenols for the treatment of T1D. The
   phytochemical profile of methanolic oregano extract (MOE) and aqueous
   oregano extract (AOE) was determined by liquid
   chromatography/electrospray ion-trap tandem MS (LC/DAD/ESI-MSn), while
   their main compounds were quantified by HPLC with diode array detection.
   After establishing their potent in vitro antioxidant activity, the
   extracts were administered to C57BL/6 mice treated with multiple low
   doses of streptozotocin for diabetes induction. While prophylactic AOE
   therapy had no impact on diabetes induction, MOE reduced diabetes
   incidence and preserved normal insulin secretion. In addition, MOE
   scavenged reactive oxygen and nitrogen species and, therefore,
   alleviated the need for the up-regulation of antioxidant enzymes. MOE
   treatment specifically attenuated the pro-inflammatory response mediated
   by T helper 17 cells and enhanced anti-inflammatory T helper 2 and T
   regulatory cells through the impact on specific signalling pathways and
   transcription factors. Importantly, MOE preserved beta-cells from in
   vitro apoptosis via blockade of caspase 3. Finally, rosmarinic acid, a
   predominant compound in MOE, exhibited only partial protection from
   diabetes induction. In conclusion, acting as an antioxidant,
   immunomodulator and in an anti-apoptotic manner, MOE protected mice from
   diabetes development. Seemingly, there is more than one compound
   responsible for the beneficial effect of MOE.",
journal = "British Journal of Nutrition",
title = "Methanolic extract of Origanum vulgare ameliorates type 1 diabetes
 through antioxidant, anti-inflammatory and anti-apoptotic activity",
number = "5",
volume = "113",
doi = "10.1017/S0007114514004048",
pages = "770-782"
}

Vujičić, M., Nikolić, I., Kontogianni, V. G., Saksida, T., Charisiadis, P., Oreščanin Dušić, Z., Blagojević, D., Stošić-Grujičić, S., Tzakos, A. G.,& Stojanović, I. D.. (2015). Methanolic extract of Origanum vulgare ameliorates type 1 diabetes
 through antioxidant, anti-inflammatory and anti-apoptotic activity. in British Journal of Nutrition, 113(5), 770-782.
https://doi.org/10.1017/S0007114514004048

Vujičić M, Nikolić I, Kontogianni VG, Saksida T, Charisiadis P, Oreščanin Dušić Z, Blagojević D, Stošić-Grujičić S, Tzakos AG, Stojanović ID. Methanolic extract of Origanum vulgare ameliorates type 1 diabetes
 through antioxidant, anti-inflammatory and anti-apoptotic activity. in British Journal of Nutrition. 2015;113(5):770-782.
doi:10.1017/S0007114514004048 .

Vujičić, Milica, Nikolić, Ivana, Kontogianni, Vassiliki G., Saksida, Tamara, Charisiadis, Pantelis, Oreščanin Dušić, Zorana, Blagojević, Duško, Stošić-Grujičić, Stanislava, Tzakos, Andreas G., Stojanović, Ivana D., "Methanolic extract of Origanum vulgare ameliorates type 1 diabetes
 through antioxidant, anti-inflammatory and anti-apoptotic activity" in British Journal of Nutrition, 113, no. 5 (2015):770-782,
https://doi.org/10.1017/S0007114514004048 . .

TY  - JOUR
AU  - Vujičić, Milica
AU  - Nikolić, Ivana
AU  - Krajnović, Tamara
AU  - Cheng, Kai-Fan
AU  - VanPatten, Sonya
AU  - He, Mingzhu
AU  - Stošić-Grujičić, Stanislava
AU  - Stojanović, Ivana D.
AU  - Al-Abed, Yousef
AU  - Saksida, Tamara
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2141
AB  - Macrophage migration inhibitory factor is a multifunctional cytokine
   involved in the regulation of immune processes and also in apoptosis
   induction. Elevated MIF expression is detrimental for insulin-producing
   beta cells and MIF inhibition protected beta cells from several
   cytotoxic insults such as inflammatory cytokines, high fatty acids or
   high glucose concentrations. Therefore, the aim of this study was to
   investigate two newly synthesized small molecule MIF inhibitors (K664-1
   and K647-1) and to compare them with previously established effects of
   the prototypical MIF inhibitor, ISO-1. Our results indicate that K664-1
   and K647-1 are 160- and 40-fold more effective in inhibition of MIF's
   tautomerase activity than ISO-1. Also, new inhibitors confer beta cell
   protection from cytokine-triggered apoptosis at significantly lower
   concentrations than LSO-1. Although all three MIF inhibitors inhibit
   caspase 3 activity, K664-1 and K647-1 suppress pro-apoptotic BAX protein
   expression and up-regulate anti-apoptotic Bcl-2 mRNA. Finally, all three
   MIF inhibitors operate through blockade of nitric oxide production
   stimulated by cytokines. In conclusion, two novel MIF inhibitors are
   more potent than ISO-1 and operate through inhibition of the
   mitochondria-related apoptotic pathway. We propose that these compounds
   represent a unique class of anti-MIF antagonists that should be further
   tested for therapeutic use. (C) 2014 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - Novel inhibitors of macrophage migration inhibitory factor prevent
 cytokine-induced beta cell death
VL  - 740
DO  - 10.1016/j.ejphar.2014.06.009
SP  - 683
EP  - 689
ER  - 

@article{
author = "Vujičić, Milica and Nikolić, Ivana and Krajnović, Tamara and Cheng, Kai-Fan and VanPatten, Sonya and He, Mingzhu and Stošić-Grujičić, Stanislava and Stojanović, Ivana D. and Al-Abed, Yousef and Saksida, Tamara",
year = "2014",
abstract = "Macrophage migration inhibitory factor is a multifunctional cytokine
   involved in the regulation of immune processes and also in apoptosis
   induction. Elevated MIF expression is detrimental for insulin-producing
   beta cells and MIF inhibition protected beta cells from several
   cytotoxic insults such as inflammatory cytokines, high fatty acids or
   high glucose concentrations. Therefore, the aim of this study was to
   investigate two newly synthesized small molecule MIF inhibitors (K664-1
   and K647-1) and to compare them with previously established effects of
   the prototypical MIF inhibitor, ISO-1. Our results indicate that K664-1
   and K647-1 are 160- and 40-fold more effective in inhibition of MIF's
   tautomerase activity than ISO-1. Also, new inhibitors confer beta cell
   protection from cytokine-triggered apoptosis at significantly lower
   concentrations than LSO-1. Although all three MIF inhibitors inhibit
   caspase 3 activity, K664-1 and K647-1 suppress pro-apoptotic BAX protein
   expression and up-regulate anti-apoptotic Bcl-2 mRNA. Finally, all three
   MIF inhibitors operate through blockade of nitric oxide production
   stimulated by cytokines. In conclusion, two novel MIF inhibitors are
   more potent than ISO-1 and operate through inhibition of the
   mitochondria-related apoptotic pathway. We propose that these compounds
   represent a unique class of anti-MIF antagonists that should be further
   tested for therapeutic use. (C) 2014 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "Novel inhibitors of macrophage migration inhibitory factor prevent
 cytokine-induced beta cell death",
volume = "740",
doi = "10.1016/j.ejphar.2014.06.009",
pages = "683-689"
}

Vujičić, M., Nikolić, I., Krajnović, T., Cheng, K., VanPatten, S., He, M., Stošić-Grujičić, S., Stojanović, I. D., Al-Abed, Y.,& Saksida, T.. (2014). Novel inhibitors of macrophage migration inhibitory factor prevent
 cytokine-induced beta cell death. in European Journal of Pharmacology, 740, 683-689.
https://doi.org/10.1016/j.ejphar.2014.06.009

Vujičić M, Nikolić I, Krajnović T, Cheng K, VanPatten S, He M, Stošić-Grujičić S, Stojanović ID, Al-Abed Y, Saksida T. Novel inhibitors of macrophage migration inhibitory factor prevent
 cytokine-induced beta cell death. in European Journal of Pharmacology. 2014;740:683-689.
doi:10.1016/j.ejphar.2014.06.009 .

Vujičić, Milica, Nikolić, Ivana, Krajnović, Tamara, Cheng, Kai-Fan, VanPatten, Sonya, He, Mingzhu, Stošić-Grujičić, Stanislava, Stojanović, Ivana D., Al-Abed, Yousef, Saksida, Tamara, "Novel inhibitors of macrophage migration inhibitory factor prevent
 cytokine-induced beta cell death" in European Journal of Pharmacology, 740 (2014):683-689,
https://doi.org/10.1016/j.ejphar.2014.06.009 . .

TY  - JOUR
AU  - Vujičić, Milica
AU  - Senerovic, Lidija
AU  - Nikolić, Ivana
AU  - Saksida, Tamara
AU  - Stošić-Grujičić, Stanislava
AU  - Stojanović, Ivana D.
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2171
AB  - Macrophage migration inhibitory factor (MIF) is a molecule with plethora
   of functions such as regulation of immune response, hormone-like,
   enzymatic and chaperone-like activity. Further, MIF is a major
   participant in glucose homeostasis since it is an autocrine stimulator
   of insulin secretion. MIF absence in male knockout mice (MW-MO) results
   in development of glucose intolerance, while sensitivity to insulin is
   fully preserved. Since our results confirm that beta cells from MIF-KO
   mice express, produce and secrete insulin similarly to beta cells of
   their wild type (WT) counterparts C57BL/6 mice, we hypothesize that
   MIF-KO-derived insulin is less active. Indeed, insulin from MIF-KO
   islets is unable to significantly induce glucose uptake into hepatocytes
   and to efficiently promote insulin-triggered Akt phosphorylation
   determined by immunoblot. However, MIF's tautomerase function is not
   crucial for insulin biosynthesis since MIF inhibitors had no impact on
   WT insulin activity. Importantly, MIF recognition by anti-MIF anti-body
   (ELISA) after in vitro co-incubation with purified insulin was
   significantly lower suggesting that insulin covers MIF immunodominant
   epitope. In addition, MIF binds insulin within beta cell as confirmed by
   co-immunoprecipitation. WT and MIF-KO-derived insulin exhibited
   different cleavage patterns suggesting different protein conformations.
   Finally, pre-incubation of recombinant MIF with insulin promotes
   formation of insulin hexamers. These results imply that MIF probably
   enables proper insulin folding what results in insulin full activity.
   This newly discovered feature of the cytokine MIF could be potentially
   important for commercially produced insulin, for increasing its
   stability and/or bioavailability. (C) 2014 Elsevier Ltd. All rights
   reserved.
T2  - Cytokine
T1  - The critical role of macrophage migration inhibitory factor in insulin
 activity
IS  - 1
VL  - 69
DO  - 10.1016/j.cyto.2014.05.013
SP  - 39
EP  - 46
ER  - 

@article{
author = "Vujičić, Milica and Senerovic, Lidija and Nikolić, Ivana and Saksida, Tamara and Stošić-Grujičić, Stanislava and Stojanović, Ivana D.",
year = "2014",
abstract = "Macrophage migration inhibitory factor (MIF) is a molecule with plethora
   of functions such as regulation of immune response, hormone-like,
   enzymatic and chaperone-like activity. Further, MIF is a major
   participant in glucose homeostasis since it is an autocrine stimulator
   of insulin secretion. MIF absence in male knockout mice (MW-MO) results
   in development of glucose intolerance, while sensitivity to insulin is
   fully preserved. Since our results confirm that beta cells from MIF-KO
   mice express, produce and secrete insulin similarly to beta cells of
   their wild type (WT) counterparts C57BL/6 mice, we hypothesize that
   MIF-KO-derived insulin is less active. Indeed, insulin from MIF-KO
   islets is unable to significantly induce glucose uptake into hepatocytes
   and to efficiently promote insulin-triggered Akt phosphorylation
   determined by immunoblot. However, MIF's tautomerase function is not
   crucial for insulin biosynthesis since MIF inhibitors had no impact on
   WT insulin activity. Importantly, MIF recognition by anti-MIF anti-body
   (ELISA) after in vitro co-incubation with purified insulin was
   significantly lower suggesting that insulin covers MIF immunodominant
   epitope. In addition, MIF binds insulin within beta cell as confirmed by
   co-immunoprecipitation. WT and MIF-KO-derived insulin exhibited
   different cleavage patterns suggesting different protein conformations.
   Finally, pre-incubation of recombinant MIF with insulin promotes
   formation of insulin hexamers. These results imply that MIF probably
   enables proper insulin folding what results in insulin full activity.
   This newly discovered feature of the cytokine MIF could be potentially
   important for commercially produced insulin, for increasing its
   stability and/or bioavailability. (C) 2014 Elsevier Ltd. All rights
   reserved.",
journal = "Cytokine",
title = "The critical role of macrophage migration inhibitory factor in insulin
 activity",
number = "1",
volume = "69",
doi = "10.1016/j.cyto.2014.05.013",
pages = "39-46"
}

Vujičić, M., Senerovic, L., Nikolić, I., Saksida, T., Stošić-Grujičić, S.,& Stojanović, I. D.. (2014). The critical role of macrophage migration inhibitory factor in insulin
 activity. in Cytokine, 69(1), 39-46.
https://doi.org/10.1016/j.cyto.2014.05.013

Vujičić M, Senerovic L, Nikolić I, Saksida T, Stošić-Grujičić S, Stojanović ID. The critical role of macrophage migration inhibitory factor in insulin
 activity. in Cytokine. 2014;69(1):39-46.
doi:10.1016/j.cyto.2014.05.013 .

Vujičić, Milica, Senerovic, Lidija, Nikolić, Ivana, Saksida, Tamara, Stošić-Grujičić, Stanislava, Stojanović, Ivana D., "The critical role of macrophage migration inhibitory factor in insulin
 activity" in Cytokine, 69, no. 1 (2014):39-46,
https://doi.org/10.1016/j.cyto.2014.05.013 . .

TY  - JOUR
AU  - Nikolić, Ivana
AU  - Saksida, Tamara
AU  - Mangano, Katia
AU  - Vujičić, Milica
AU  - Stojanović, Ivana D.
AU  - Nicoletti, Ferdinando
AU  - Stošić-Grujičić, Stanislava
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2221
AB  - Aims/hypothesis Recent studies have identified carbon monoxide (CO) as a
   potential therapeutic molecule for the treatment of autoimmune diseases
   owing to its anti-inflammatory and anti-apoptotic properties. We
   explored the efficacy and the mechanisms of action of the CO-releasing
   molecule (CORM)-A1 in preclinical models of type 1 diabetes.
   Methods The impact of CORM-A1 on diabetes development was evaluated in
   models of spontaneous diabetes in NOD mice and in diabetes induced in
   C57BL/6 mice by multiple low-dose streptozotocin (MLDS). Ex vivo
   analysis was performed to determine the impact of CORM-A1 both on T
   helper (Th) cell and macrophage differentiation and on their production
   of soluble mediators in peripheral tissues and in infiltrates of
   pancreatic islets. The potential effect of CORM-A1 on cytokine-induced
   apoptosis in pancreatic islets or beta cells was evaluated in vitro.
   Results CORM-A1 conferred protection from diabetes in MLDS-induced mice
   and reduced diabetes incidence in NOD mice as confirmed by preserved
   insulin secretion and improved histological signs of the disease. In
   MLDS-challenged mice, CORM-A1 attenuated Th1, Th17, and M1 macrophage
   response and facilitated Th2 cell differentiation. In addition, CORM-A1
   treatment in NOD mice upregulated the regulatory arm of the immune
   response (M2 macrophages and FoxP3(+) regulatory T cells). Importantly,
   CORM-A1 interfered with in vitro cytokine-induced beta cell apoptosis
   through the reduction of cytochrome c and caspase 3 levels.
   Conclusions/interpretation The ability of CORM-A1 to protect mice from
   developing type 1 diabetes provides a valuable proof of concept for the
   potential exploitation of controlled CO delivery in clinical settings
   for the treatment of autoimmune diabetes.
T2  - Diabetologia
T1  - Pharmacological application of carbon monoxide ameliorates
 islet-directed autoimmunity in mice via anti-inflammatory and
 anti-apoptotic effects
IS  - 5
VL  - 57
DO  - 10.1007/s00125-014-3170-7
SP  - 980
EP  - 990
ER  - 

@article{
author = "Nikolić, Ivana and Saksida, Tamara and Mangano, Katia and Vujičić, Milica and Stojanović, Ivana D. and Nicoletti, Ferdinando and Stošić-Grujičić, Stanislava",
year = "2014",
abstract = "Aims/hypothesis Recent studies have identified carbon monoxide (CO) as a
   potential therapeutic molecule for the treatment of autoimmune diseases
   owing to its anti-inflammatory and anti-apoptotic properties. We
   explored the efficacy and the mechanisms of action of the CO-releasing
   molecule (CORM)-A1 in preclinical models of type 1 diabetes.
   Methods The impact of CORM-A1 on diabetes development was evaluated in
   models of spontaneous diabetes in NOD mice and in diabetes induced in
   C57BL/6 mice by multiple low-dose streptozotocin (MLDS). Ex vivo
   analysis was performed to determine the impact of CORM-A1 both on T
   helper (Th) cell and macrophage differentiation and on their production
   of soluble mediators in peripheral tissues and in infiltrates of
   pancreatic islets. The potential effect of CORM-A1 on cytokine-induced
   apoptosis in pancreatic islets or beta cells was evaluated in vitro.
   Results CORM-A1 conferred protection from diabetes in MLDS-induced mice
   and reduced diabetes incidence in NOD mice as confirmed by preserved
   insulin secretion and improved histological signs of the disease. In
   MLDS-challenged mice, CORM-A1 attenuated Th1, Th17, and M1 macrophage
   response and facilitated Th2 cell differentiation. In addition, CORM-A1
   treatment in NOD mice upregulated the regulatory arm of the immune
   response (M2 macrophages and FoxP3(+) regulatory T cells). Importantly,
   CORM-A1 interfered with in vitro cytokine-induced beta cell apoptosis
   through the reduction of cytochrome c and caspase 3 levels.
   Conclusions/interpretation The ability of CORM-A1 to protect mice from
   developing type 1 diabetes provides a valuable proof of concept for the
   potential exploitation of controlled CO delivery in clinical settings
   for the treatment of autoimmune diabetes.",
journal = "Diabetologia",
title = "Pharmacological application of carbon monoxide ameliorates
 islet-directed autoimmunity in mice via anti-inflammatory and
 anti-apoptotic effects",
number = "5",
volume = "57",
doi = "10.1007/s00125-014-3170-7",
pages = "980-990"
}

Nikolić, I., Saksida, T., Mangano, K., Vujičić, M., Stojanović, I. D., Nicoletti, F.,& Stošić-Grujičić, S.. (2014). Pharmacological application of carbon monoxide ameliorates
 islet-directed autoimmunity in mice via anti-inflammatory and
 anti-apoptotic effects. in Diabetologia, 57(5), 980-990.
https://doi.org/10.1007/s00125-014-3170-7

Nikolić I, Saksida T, Mangano K, Vujičić M, Stojanović ID, Nicoletti F, Stošić-Grujičić S. Pharmacological application of carbon monoxide ameliorates
 islet-directed autoimmunity in mice via anti-inflammatory and
 anti-apoptotic effects. in Diabetologia. 2014;57(5):980-990.
doi:10.1007/s00125-014-3170-7 .

Nikolić, Ivana, Saksida, Tamara, Mangano, Katia, Vujičić, Milica, Stojanović, Ivana D., Nicoletti, Ferdinando, Stošić-Grujičić, Stanislava, "Pharmacological application of carbon monoxide ameliorates
 islet-directed autoimmunity in mice via anti-inflammatory and
 anti-apoptotic effects" in Diabetologia, 57, no. 5 (2014):980-990,
https://doi.org/10.1007/s00125-014-3170-7 . .

TY  - JOUR
AU  - Saksida, Tamara
AU  - Vujičić, Milica
AU  - Nikolić, Ivana
AU  - Stojanović, Ivana D.
AU  - Haegeman, G.
AU  - Stošić-Grujičić, Stanislava
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2111
AB  - Background and PurposeType 1 diabetes is a multifactorial inflammatory
   disease that develops as a result of deregulated immune responses,
   causing progressive autoimmune destruction of insulin-producing beta
   cells of pancreas. 2-((4-acetoxyphenyl)-2-chloro-N-methyl) ethylammonium
   chloride, compound A (CpdA), is a selective glucocorticoid receptor (GR)
   agonist that displays strong anti-inflammatory and immunomodulatory
   activities. We investigated the therapeutic effectiveness of CpdA in a
   pharmacological model of type 1 diabetes in mice.
   Experimental ApproachThe utility of CpdA in diabetes prevention was
   evaluated in vivo through its prophylactic administration to male
   C57BL/6 mice that received multiple low doses of streptozotocin for
   immunoinflammatory diabetes induction. The effect of CpdA on disease
   development was studied by measuring blood glucose and insulin level,
   histopathological examination, determination of the nature of
   infiltrating cells, pro- and anti-inflammatory cytokine production, and
   signalling pathways.
   Key ResultsProphylactic in vivo therapy with CpdA conferred protection
   against development of immunoinflammatory diabetes in mice by dampening
   the M1/Th1/Th17 immune response and switching it towards an
   anti-inflammatory M2/Th2/Treg profile, thus preserving beta cell
   function.
   Conclusions and ImplicationsAnti-diabetic properties of CpdA are
   mediated through modulation of immune cell-mediated pathways, but
   without triggering adverse events. These findings provide basic
   information for the therapeutic use of selective GR agonists in the
   amelioration of islet-directed autoimmunity.
T2  - British Journal of Pharmacology
T1  - Compound A, a selective glucocorticoid receptor agonist, inhibits
 immunoinflammatory diabetes, induced by multiple low doses of
 streptozotocin in mice
IS  - 24, SI
VL  - 171
DO  - 10.1111/bph.12892
SP  - 5898
EP  - 5909
ER  - 

@article{
author = "Saksida, Tamara and Vujičić, Milica and Nikolić, Ivana and Stojanović, Ivana D. and Haegeman, G. and Stošić-Grujičić, Stanislava",
year = "2014",
abstract = "Background and PurposeType 1 diabetes is a multifactorial inflammatory
   disease that develops as a result of deregulated immune responses,
   causing progressive autoimmune destruction of insulin-producing beta
   cells of pancreas. 2-((4-acetoxyphenyl)-2-chloro-N-methyl) ethylammonium
   chloride, compound A (CpdA), is a selective glucocorticoid receptor (GR)
   agonist that displays strong anti-inflammatory and immunomodulatory
   activities. We investigated the therapeutic effectiveness of CpdA in a
   pharmacological model of type 1 diabetes in mice.
   Experimental ApproachThe utility of CpdA in diabetes prevention was
   evaluated in vivo through its prophylactic administration to male
   C57BL/6 mice that received multiple low doses of streptozotocin for
   immunoinflammatory diabetes induction. The effect of CpdA on disease
   development was studied by measuring blood glucose and insulin level,
   histopathological examination, determination of the nature of
   infiltrating cells, pro- and anti-inflammatory cytokine production, and
   signalling pathways.
   Key ResultsProphylactic in vivo therapy with CpdA conferred protection
   against development of immunoinflammatory diabetes in mice by dampening
   the M1/Th1/Th17 immune response and switching it towards an
   anti-inflammatory M2/Th2/Treg profile, thus preserving beta cell
   function.
   Conclusions and ImplicationsAnti-diabetic properties of CpdA are
   mediated through modulation of immune cell-mediated pathways, but
   without triggering adverse events. These findings provide basic
   information for the therapeutic use of selective GR agonists in the
   amelioration of islet-directed autoimmunity.",
journal = "British Journal of Pharmacology",
title = "Compound A, a selective glucocorticoid receptor agonist, inhibits
 immunoinflammatory diabetes, induced by multiple low doses of
 streptozotocin in mice",
number = "24, SI",
volume = "171",
doi = "10.1111/bph.12892",
pages = "5898-5909"
}

Saksida, T., Vujičić, M., Nikolić, I., Stojanović, I. D., Haegeman, G.,& Stošić-Grujičić, S.. (2014). Compound A, a selective glucocorticoid receptor agonist, inhibits
 immunoinflammatory diabetes, induced by multiple low doses of
 streptozotocin in mice. in British Journal of Pharmacology, 171(24, SI), 5898-5909.
https://doi.org/10.1111/bph.12892

Saksida T, Vujičić M, Nikolić I, Stojanović ID, Haegeman G, Stošić-Grujičić S. Compound A, a selective glucocorticoid receptor agonist, inhibits
 immunoinflammatory diabetes, induced by multiple low doses of
 streptozotocin in mice. in British Journal of Pharmacology. 2014;171(24, SI):5898-5909.
doi:10.1111/bph.12892 .

Saksida, Tamara, Vujičić, Milica, Nikolić, Ivana, Stojanović, Ivana D., Haegeman, G., Stošić-Grujičić, Stanislava, "Compound A, a selective glucocorticoid receptor agonist, inhibits
 immunoinflammatory diabetes, induced by multiple low doses of
 streptozotocin in mice" in British Journal of Pharmacology, 171, no. 24, SI (2014):5898-5909,
https://doi.org/10.1111/bph.12892 . .

TY  - JOUR
AU  - Nikolić, Ivana
AU  - Vujičić, Milica
AU  - Stojanović, Ivana D.
AU  - Stošić-Grujičić, Stanislava
AU  - Saksida, Tamara
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2183
AB  - Carbon monoxide (CO) is endogenously produced by haeme oxygenase-1 and
   has profound effects on intracellular signalling processes, generating
   anti-inflammatory, antiproliferative and antiapoptotic effects. A
   boron-containing compound CORM-A1 is capable of releasing CO in such a
   way to mimic physiological functions of haeme oxygenase-1. Considering
   the importance of Th1/Th17 versus Th2 balance in the final outcome of
   immune and inflammatory responses in this study we focused on
   immune-modulatory effects of CORM-A1 on murine lymph node-derived T
   cells in vitro and its influence on T-cell proliferation, activation and
   differentiation. Anti-CD3/CD28 antibody-triggered lymph node cells
   proliferation remained unaffected after 24-hour CORM-A1 treatment, as
   well as the expression of the early activation marker CD25. However,
   CORM-A1 successfully reduced the secretion of the two representative
   pro-inflammatory cytokines, IFN-gamma and IL-17, while the secretion of
   anti-inflammatory cytokine IL-4 remained unchanged. Furthermore, CORM-A1
   efficiently reduced the percentage of CD4(+)IFN-gamma(+) and
   CD4(+)IL-17(+) cells, whereas CD4(+)IL-4(+) cell population increased
   after treatment. Also, CORM-A1 significantly reduced expression of
   transcription factor ROR gamma T, necessary for Th17 development, but
   the expression of Th1-related and Th2-related transcription factors
   (T-bet and GATA-3, respectively) remained unchanged. In conclusion, our
   findings indicate that CO has anti-inflammatory role through the
   regulation of balance between pro-inflammatory Th1/Th17 and
   anti-inflammatory Th2 cells. Observed immunomodulatory effects of
   CORM-A1 could be useful for developing novel therapeutic approaches in
   managing Th1/Th17-mediated immune disorders.
T2  - Scandinavian Journal of Immunology
T1  - Carbon Monoxide-Releasing Molecule-A1 Inhibits Th1/Th17 and Stimulates
 Th2 Differentiation In vitro
IS  - 2
VL  - 80
DO  - 10.1111/sji.12189
SP  - 95
EP  - 100
ER  - 

@article{
author = "Nikolić, Ivana and Vujičić, Milica and Stojanović, Ivana D. and Stošić-Grujičić, Stanislava and Saksida, Tamara",
year = "2014",
abstract = "Carbon monoxide (CO) is endogenously produced by haeme oxygenase-1 and
   has profound effects on intracellular signalling processes, generating
   anti-inflammatory, antiproliferative and antiapoptotic effects. A
   boron-containing compound CORM-A1 is capable of releasing CO in such a
   way to mimic physiological functions of haeme oxygenase-1. Considering
   the importance of Th1/Th17 versus Th2 balance in the final outcome of
   immune and inflammatory responses in this study we focused on
   immune-modulatory effects of CORM-A1 on murine lymph node-derived T
   cells in vitro and its influence on T-cell proliferation, activation and
   differentiation. Anti-CD3/CD28 antibody-triggered lymph node cells
   proliferation remained unaffected after 24-hour CORM-A1 treatment, as
   well as the expression of the early activation marker CD25. However,
   CORM-A1 successfully reduced the secretion of the two representative
   pro-inflammatory cytokines, IFN-gamma and IL-17, while the secretion of
   anti-inflammatory cytokine IL-4 remained unchanged. Furthermore, CORM-A1
   efficiently reduced the percentage of CD4(+)IFN-gamma(+) and
   CD4(+)IL-17(+) cells, whereas CD4(+)IL-4(+) cell population increased
   after treatment. Also, CORM-A1 significantly reduced expression of
   transcription factor ROR gamma T, necessary for Th17 development, but
   the expression of Th1-related and Th2-related transcription factors
   (T-bet and GATA-3, respectively) remained unchanged. In conclusion, our
   findings indicate that CO has anti-inflammatory role through the
   regulation of balance between pro-inflammatory Th1/Th17 and
   anti-inflammatory Th2 cells. Observed immunomodulatory effects of
   CORM-A1 could be useful for developing novel therapeutic approaches in
   managing Th1/Th17-mediated immune disorders.",
journal = "Scandinavian Journal of Immunology",
title = "Carbon Monoxide-Releasing Molecule-A1 Inhibits Th1/Th17 and Stimulates
 Th2 Differentiation In vitro",
number = "2",
volume = "80",
doi = "10.1111/sji.12189",
pages = "95-100"
}

Nikolić, I., Vujičić, M., Stojanović, I. D., Stošić-Grujičić, S.,& Saksida, T.. (2014). Carbon Monoxide-Releasing Molecule-A1 Inhibits Th1/Th17 and Stimulates
 Th2 Differentiation In vitro. in Scandinavian Journal of Immunology, 80(2), 95-100.
https://doi.org/10.1111/sji.12189

Nikolić I, Vujičić M, Stojanović ID, Stošić-Grujičić S, Saksida T. Carbon Monoxide-Releasing Molecule-A1 Inhibits Th1/Th17 and Stimulates
 Th2 Differentiation In vitro. in Scandinavian Journal of Immunology. 2014;80(2):95-100.
doi:10.1111/sji.12189 .

Nikolić, Ivana, Vujičić, Milica, Stojanović, Ivana D., Stošić-Grujičić, Stanislava, Saksida, Tamara, "Carbon Monoxide-Releasing Molecule-A1 Inhibits Th1/Th17 and Stimulates
 Th2 Differentiation In vitro" in Scandinavian Journal of Immunology, 80, no. 2 (2014):95-100,
https://doi.org/10.1111/sji.12189 . .

TY  - JOUR
AU  - Kontogianni, Vassiliki G
AU  - Tomić, Goran
AU  - Nikolić, Ivana
AU  - Nerantzaki, Alexandra A
AU  - Sayyad, Nisar
AU  - Stošić-Grujičić, Stanislava
AU  - Stojanović, Ivana D.
AU  - Gerothanassis, Ioannis P
AU  - Tzakos, Andreas G
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1068
AB  - The goal of this study was to monitor the anti-proliferative activity of Rosmarinus officinalis and Salvia officinalis extracts against cancer cells and to correlate this activity with their phytochemical profiles using liquid chromatography/diode array detection/electrospray ion trap tandem mass spectrometry (LC/DAD/ESI-MSn). For the quantitative estimation of triterpenic acids in the crude extracts an NMR based methodology was used and compared with the HPLC measurements, both applied for the first time, for the case of betulinic acid. Both extracts exerted cytotoxic activity through dose-dependent impairment of viability and mitochondrial activity of rat insulinoma m5F (RINm5F) cells. Decrease of RINm5F viability was mediated by nitric oxide (NO)-induced apoptosis. Importantly, these extracts potentiated NO and TNF-alpha release from macrophages therefore enhancing their cytocidal action. The rosemary extract developed more pronounced antioxidant, cytotoxic and immunomodifying activities, probably due to the presence of betulinic acid and a higher concentration of carnosic acid in its phytochemical profile. (C) 2012 Elsevier Ltd. All rights reserved.
T2  - Food Chemistry
T1  - Phytochemical profile of Rosmarinus officinalis and Salvia officinalis extracts and correlation to their antioxidant and anti-proliferative activity
IS  - 1
VL  - 136
DO  - 10.1016/j.foodchem.2012.07.091
SP  - 385
EP  - 129
ER  - 

@article{
author = "Kontogianni, Vassiliki G and Tomić, Goran and Nikolić, Ivana and Nerantzaki, Alexandra A and Sayyad, Nisar and Stošić-Grujičić, Stanislava and Stojanović, Ivana D. and Gerothanassis, Ioannis P and Tzakos, Andreas G",
year = "2013",
abstract = "The goal of this study was to monitor the anti-proliferative activity of Rosmarinus officinalis and Salvia officinalis extracts against cancer cells and to correlate this activity with their phytochemical profiles using liquid chromatography/diode array detection/electrospray ion trap tandem mass spectrometry (LC/DAD/ESI-MSn). For the quantitative estimation of triterpenic acids in the crude extracts an NMR based methodology was used and compared with the HPLC measurements, both applied for the first time, for the case of betulinic acid. Both extracts exerted cytotoxic activity through dose-dependent impairment of viability and mitochondrial activity of rat insulinoma m5F (RINm5F) cells. Decrease of RINm5F viability was mediated by nitric oxide (NO)-induced apoptosis. Importantly, these extracts potentiated NO and TNF-alpha release from macrophages therefore enhancing their cytocidal action. The rosemary extract developed more pronounced antioxidant, cytotoxic and immunomodifying activities, probably due to the presence of betulinic acid and a higher concentration of carnosic acid in its phytochemical profile. (C) 2012 Elsevier Ltd. All rights reserved.",
journal = "Food Chemistry",
title = "Phytochemical profile of Rosmarinus officinalis and Salvia officinalis extracts and correlation to their antioxidant and anti-proliferative activity",
number = "1",
volume = "136",
doi = "10.1016/j.foodchem.2012.07.091",
pages = "385-129"
}

Kontogianni, V. G., Tomić, G., Nikolić, I., Nerantzaki, A. A., Sayyad, N., Stošić-Grujičić, S., Stojanović, I. D., Gerothanassis, I. P.,& Tzakos, A. G.. (2013). Phytochemical profile of Rosmarinus officinalis and Salvia officinalis extracts and correlation to their antioxidant and anti-proliferative activity. in Food Chemistry, 136(1), 385-129.
https://doi.org/10.1016/j.foodchem.2012.07.091

Kontogianni VG, Tomić G, Nikolić I, Nerantzaki AA, Sayyad N, Stošić-Grujičić S, Stojanović ID, Gerothanassis IP, Tzakos AG. Phytochemical profile of Rosmarinus officinalis and Salvia officinalis extracts and correlation to their antioxidant and anti-proliferative activity. in Food Chemistry. 2013;136(1):385-129.
doi:10.1016/j.foodchem.2012.07.091 .

Kontogianni, Vassiliki G, Tomić, Goran, Nikolić, Ivana, Nerantzaki, Alexandra A, Sayyad, Nisar, Stošić-Grujičić, Stanislava, Stojanović, Ivana D., Gerothanassis, Ioannis P, Tzakos, Andreas G, "Phytochemical profile of Rosmarinus officinalis and Salvia officinalis extracts and correlation to their antioxidant and anti-proliferative activity" in Food Chemistry, 136, no. 1 (2013):385-129,
https://doi.org/10.1016/j.foodchem.2012.07.091 . .

TY  - JOUR
AU  - Pejin, Boris
AU  - Stošić-Grujičić, Stanislava
AU  - Bogdanović, Gordana M
AU  - Hegedis, Aleksandar E
AU  - Karaman, Ivo M
AU  - Stojanović, Ivana D.
AU  - Nikolić, Ivana
AU  - Kojić, Vesna V
AU  - Horvatović, Mladen
AU  - Radotić, Ksenija
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1060
AB  - The immunomodulatory and anticarcinogenic activity of the freshwater bryozoan Hyalinella punctata methanolic extract (MEx) was evaluated in vitro on selected biosystems for the first time. Murine lymphocytes and macrophages were used for testing of MEx effects on cell proliferation and nitric oxide (NO) production, respectively, while human cancer cell lines were utilized for measuring its activity against cancer cells. The results suggest a strong and tissue-specific immunomodifying activity (IC50 values for inhibition of proliferation of lymph node and spleen-derived lymphocytes were 4.1 mu g/ml and 9.7 mu g/ml, respectively) and moderate anticancer activity of MEx (IC50 value for the MCF-7 cell line was 24.13 mu g/ml). Down-regulation of macrophage NO production was also obtained. The potential use of H. punctata-derived natural products for the treatment of human chronic inflammatory diseases and cancer is worthy of further investigation.
T2  - Digest Journal of Nanomaterials and Biostructures
T1  - In Vitro Evaluation of the Immunomodulatory and Anticarcinogenic Activity of the Freshwater Bryozoan Hyalinella Punctata Methanolic Extract
IS  - 1
VL  - 8
SP  - 301
EP  - 195
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1060
ER  - 

@article{
author = "Pejin, Boris and Stošić-Grujičić, Stanislava and Bogdanović, Gordana M and Hegedis, Aleksandar E and Karaman, Ivo M and Stojanović, Ivana D. and Nikolić, Ivana and Kojić, Vesna V and Horvatović, Mladen and Radotić, Ksenija",
year = "2013",
abstract = "The immunomodulatory and anticarcinogenic activity of the freshwater bryozoan Hyalinella punctata methanolic extract (MEx) was evaluated in vitro on selected biosystems for the first time. Murine lymphocytes and macrophages were used for testing of MEx effects on cell proliferation and nitric oxide (NO) production, respectively, while human cancer cell lines were utilized for measuring its activity against cancer cells. The results suggest a strong and tissue-specific immunomodifying activity (IC50 values for inhibition of proliferation of lymph node and spleen-derived lymphocytes were 4.1 mu g/ml and 9.7 mu g/ml, respectively) and moderate anticancer activity of MEx (IC50 value for the MCF-7 cell line was 24.13 mu g/ml). Down-regulation of macrophage NO production was also obtained. The potential use of H. punctata-derived natural products for the treatment of human chronic inflammatory diseases and cancer is worthy of further investigation.",
journal = "Digest Journal of Nanomaterials and Biostructures",
title = "In Vitro Evaluation of the Immunomodulatory and Anticarcinogenic Activity of the Freshwater Bryozoan Hyalinella Punctata Methanolic Extract",
number = "1",
volume = "8",
pages = "301-195",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1060"
}

Pejin, B., Stošić-Grujičić, S., Bogdanović, G. M., Hegedis, A. E., Karaman, I. M., Stojanović, I. D., Nikolić, I., Kojić, V. V., Horvatović, M.,& Radotić, K.. (2013). In Vitro Evaluation of the Immunomodulatory and Anticarcinogenic Activity of the Freshwater Bryozoan Hyalinella Punctata Methanolic Extract. in Digest Journal of Nanomaterials and Biostructures, 8(1), 301-195.
https://hdl.handle.net/21.15107/rcub_ibiss_1060

Pejin B, Stošić-Grujičić S, Bogdanović GM, Hegedis AE, Karaman IM, Stojanović ID, Nikolić I, Kojić VV, Horvatović M, Radotić K. In Vitro Evaluation of the Immunomodulatory and Anticarcinogenic Activity of the Freshwater Bryozoan Hyalinella Punctata Methanolic Extract. in Digest Journal of Nanomaterials and Biostructures. 2013;8(1):301-195.
https://hdl.handle.net/21.15107/rcub_ibiss_1060 .

Pejin, Boris, Stošić-Grujičić, Stanislava, Bogdanović, Gordana M, Hegedis, Aleksandar E, Karaman, Ivo M, Stojanović, Ivana D., Nikolić, Ivana, Kojić, Vesna V, Horvatović, Mladen, Radotić, Ksenija, "In Vitro Evaluation of the Immunomodulatory and Anticarcinogenic Activity of the Freshwater Bryozoan Hyalinella Punctata Methanolic Extract" in Digest Journal of Nanomaterials and Biostructures, 8, no. 1 (2013):301-195,
https://hdl.handle.net/21.15107/rcub_ibiss_1060 .

TY  - JOUR
AU  - Saksida, Tamara
AU  - Nikolić, Ivana
AU  - Vujičić, Milica
AU  - Nilsson, Ulf J
AU  - Leffler, Hakon
AU  - Lukić, Miodrag L
AU  - Stojanović, Ivana D.
AU  - Stošić-Grujičić, Stanislava
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/995
AB  - Beta cell apoptosis is a hallmark of diabetes. Since we have previously shown that galectin-3 deficient (LGALS3/) mice are relatively resistant to diabetes induction, the aim of this study was to examine whether beta cell apoptosis depends on the presence of galectin-3 and to delineate the underlying mechanism. Deficiency of galectin-3, either hereditary or induced through application of chemical inhibitors, -lactose or TD139, supported survival and function of islet beta cells compromised by TNF-+IFN-+IL-1 stimulus. Similarly, inhibition of galectin-3 by -lactose or TD139 reduced cytokine-triggered apoptosis of beta cells, leading to conclusion that endogenous galectin-3 propagates beta apoptosis in the presence of an inflammatory milieu. Exploring apoptosis-related molecules expression in primary islet cells before and after treatment with cytokines we found that galectin-3 ablation affected the expression of major components of mitochondrial apoptotic pathway, such as BAX, caspase-9, Apaf, SMAC, caspase-3, and AIF. In contrast, anti-apoptotic molecules Bcl-2 and Bcl-XL were up-regulated in LGALS3/ islet cells when compared to wild-type (WT) counterparts (C57BL/6), resulting in increased ratio of anti-apoptotic versus pro-apoptotic molecules. However, Fas-triggered apoptotic pathway as well as extracellular signal-regulated kinase 1/2 (ERK1/2) was not influenced by LGALS-3 deletion. All together, these results point to an important role of endogenous galectin-3 in beta cell apoptosis in the inflammatory milieu that occurs during diabetes pathogenesis and implicates impairment of mitochondrial apoptotic pathway as a key event in protection from beta cell apoptosis in the absence of galectin-3. J. Cell. Physiol. 228: 15681576, 2013. (c) 2012 Wiley Periodicals, Inc.
T2  - Journal of Cellular Physiology
T1  - Galectin-3 deficiency protects pancreatic islet cells from cytokine-triggered apoptosis in vitro
IS  - 7
VL  - 228
SP  - 25
EP  - 1576
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_995
ER  - 

@article{
author = "Saksida, Tamara and Nikolić, Ivana and Vujičić, Milica and Nilsson, Ulf J and Leffler, Hakon and Lukić, Miodrag L and Stojanović, Ivana D. and Stošić-Grujičić, Stanislava",
year = "2013",
abstract = "Beta cell apoptosis is a hallmark of diabetes. Since we have previously shown that galectin-3 deficient (LGALS3/) mice are relatively resistant to diabetes induction, the aim of this study was to examine whether beta cell apoptosis depends on the presence of galectin-3 and to delineate the underlying mechanism. Deficiency of galectin-3, either hereditary or induced through application of chemical inhibitors, -lactose or TD139, supported survival and function of islet beta cells compromised by TNF-+IFN-+IL-1 stimulus. Similarly, inhibition of galectin-3 by -lactose or TD139 reduced cytokine-triggered apoptosis of beta cells, leading to conclusion that endogenous galectin-3 propagates beta apoptosis in the presence of an inflammatory milieu. Exploring apoptosis-related molecules expression in primary islet cells before and after treatment with cytokines we found that galectin-3 ablation affected the expression of major components of mitochondrial apoptotic pathway, such as BAX, caspase-9, Apaf, SMAC, caspase-3, and AIF. In contrast, anti-apoptotic molecules Bcl-2 and Bcl-XL were up-regulated in LGALS3/ islet cells when compared to wild-type (WT) counterparts (C57BL/6), resulting in increased ratio of anti-apoptotic versus pro-apoptotic molecules. However, Fas-triggered apoptotic pathway as well as extracellular signal-regulated kinase 1/2 (ERK1/2) was not influenced by LGALS-3 deletion. All together, these results point to an important role of endogenous galectin-3 in beta cell apoptosis in the inflammatory milieu that occurs during diabetes pathogenesis and implicates impairment of mitochondrial apoptotic pathway as a key event in protection from beta cell apoptosis in the absence of galectin-3. J. Cell. Physiol. 228: 15681576, 2013. (c) 2012 Wiley Periodicals, Inc.",
journal = "Journal of Cellular Physiology",
title = "Galectin-3 deficiency protects pancreatic islet cells from cytokine-triggered apoptosis in vitro",
number = "7",
volume = "228",
pages = "25-1576",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_995"
}

Saksida, T., Nikolić, I., Vujičić, M., Nilsson, U. J., Leffler, H., Lukić, M. L., Stojanović, I. D.,& Stošić-Grujičić, S.. (2013). Galectin-3 deficiency protects pancreatic islet cells from cytokine-triggered apoptosis in vitro. in Journal of Cellular Physiology, 228(7), 25-1576.
https://hdl.handle.net/21.15107/rcub_ibiss_995

Saksida T, Nikolić I, Vujičić M, Nilsson UJ, Leffler H, Lukić ML, Stojanović ID, Stošić-Grujičić S. Galectin-3 deficiency protects pancreatic islet cells from cytokine-triggered apoptosis in vitro. in Journal of Cellular Physiology. 2013;228(7):25-1576.
https://hdl.handle.net/21.15107/rcub_ibiss_995 .

Saksida, Tamara, Nikolić, Ivana, Vujičić, Milica, Nilsson, Ulf J, Leffler, Hakon, Lukić, Miodrag L, Stojanović, Ivana D., Stošić-Grujičić, Stanislava, "Galectin-3 deficiency protects pancreatic islet cells from cytokine-triggered apoptosis in vitro" in Journal of Cellular Physiology, 228, no. 7 (2013):25-1576,
https://hdl.handle.net/21.15107/rcub_ibiss_995 .

TY  - CONF
AU  - Nikolić, Ivana
AU  - Saksida, Tamara
AU  - Berki, Timea
AU  - Stošić-Grujičić, Stanislava
AU  - Stojanović, Ivana D.
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/989
C3  - Febs Journal
T1  - The role of endogenous glucocorticoids in glucose metabolism and immune status of MIF-deficient mice
IS  - null
VL  - 280
SP  - 142
EP  - 455
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_989
ER  - 

@conference{
author = "Nikolić, Ivana and Saksida, Tamara and Berki, Timea and Stošić-Grujičić, Stanislava and Stojanović, Ivana D.",
year = "2013",
journal = "Febs Journal",
title = "The role of endogenous glucocorticoids in glucose metabolism and immune status of MIF-deficient mice",
number = "null",
volume = "280",
pages = "142-455",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_989"
}

Nikolić, I., Saksida, T., Berki, T., Stošić-Grujičić, S.,& Stojanović, I. D.. (2013). The role of endogenous glucocorticoids in glucose metabolism and immune status of MIF-deficient mice. in Febs Journal, 280(null), 142-455.
https://hdl.handle.net/21.15107/rcub_ibiss_989

Nikolić I, Saksida T, Berki T, Stošić-Grujičić S, Stojanović ID. The role of endogenous glucocorticoids in glucose metabolism and immune status of MIF-deficient mice. in Febs Journal. 2013;280(null):142-455.
https://hdl.handle.net/21.15107/rcub_ibiss_989 .

Nikolić, Ivana, Saksida, Tamara, Berki, Timea, Stošić-Grujičić, Stanislava, Stojanović, Ivana D., "The role of endogenous glucocorticoids in glucose metabolism and immune status of MIF-deficient mice" in Febs Journal, 280, no. null (2013):142-455,
https://hdl.handle.net/21.15107/rcub_ibiss_989 .

TY  - CONF
AU  - Nikolić, Ivana
AU  - Saksida, Tamara
AU  - Vujičić, Milica
AU  - Stojanović, Ivana D.
AU  - Nicoletti, Ferdinando
AU  - Stošić-Grujičić, Stanislava
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/966
C3  - Diabetologia
T1  - Carbon monoxide-releasing molecule CORM-A1 ameliorates islet-directed autoimmunity in mice
IS  - null
VL  - 56
SP  - 39
EP  - S228
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_966
ER  - 

@conference{
author = "Nikolić, Ivana and Saksida, Tamara and Vujičić, Milica and Stojanović, Ivana D. and Nicoletti, Ferdinando and Stošić-Grujičić, Stanislava",
year = "2013",
journal = "Diabetologia",
title = "Carbon monoxide-releasing molecule CORM-A1 ameliorates islet-directed autoimmunity in mice",
number = "null",
volume = "56",
pages = "39-S228",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_966"
}

Nikolić, I., Saksida, T., Vujičić, M., Stojanović, I. D., Nicoletti, F.,& Stošić-Grujičić, S.. (2013). Carbon monoxide-releasing molecule CORM-A1 ameliorates islet-directed autoimmunity in mice. in Diabetologia, 56(null), 39-S228.
https://hdl.handle.net/21.15107/rcub_ibiss_966

Nikolić I, Saksida T, Vujičić M, Stojanović ID, Nicoletti F, Stošić-Grujičić S. Carbon monoxide-releasing molecule CORM-A1 ameliorates islet-directed autoimmunity in mice. in Diabetologia. 2013;56(null):39-S228.
https://hdl.handle.net/21.15107/rcub_ibiss_966 .

Nikolić, Ivana, Saksida, Tamara, Vujičić, Milica, Stojanović, Ivana D., Nicoletti, Ferdinando, Stošić-Grujičić, Stanislava, "Carbon monoxide-releasing molecule CORM-A1 ameliorates islet-directed autoimmunity in mice" in Diabetologia, 56, no. null (2013):39-S228,
https://hdl.handle.net/21.15107/rcub_ibiss_966 .

TY  - JOUR
AU  - Pejnović, Nada N
AU  - Pantić, Jelena M
AU  - Jovanović, Ivan P
AU  - Radosavljević, Gordana D
AU  - Milovanović, Marija Z
AU  - Nikolić, Ivana
AU  - Zdravković, Nemanja S
AU  - Đukić, Aleksandar Lj
AU  - Arsenijević, Nebojsa N
AU  - Lukić, Miodrag L
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1003
AB  - Obesity-induced diabetes is associated with low-grade inflammation in adipose tissue and macrophage infiltration of islets. We show that ablation of galectin-3 (Gal-3), a galactoside-binding lectin, accelerates high-fat diet-induced obesity and diabetes. Obese LGALS3(-/-) mice have increased body weight, amount of total visceral adipose tissue (VAT), fasting blood glucose and insulin levels, homeostasis model assessment of insulin resistance, and markers of systemic inflammation compared with diet-matched wild-type (WT) animals. VAT of obese LGALS3(-/-) mice exhibited increased incidence of type 1 T and NKT lymphocytes and proinflammatory CD11c(+)CD11b(+) macrophages and decreased CD4(+)CD25(+)FoxP3(+) regulatory T cells and M2 macrophages. Pronounced mononuclear cell infiltrate, increased expression of NLRP3 inflammasome and interleukin-1 beta (IL-1 beta) in macrophages, and increased accumulation of advanced glycation end products (AGEs) and receptor for AGE (RAGE) expression were present in pancreatic islets of obese LGALS3(-/-) animals accompanied with elevated phosphorylated nuclear factor-kappa B (NF-kappa B) p65 and mature caspase-1 protein expression in pancreatic tissue and VAT. In vitro stimulation of LGALS3(-/-) peritoneal macrophages with lipopolysaccharide (LPS) and saturated fatty acid palmitate caused increased caspase-l-dependent IL-1 beta production and increased phosphorylation of NF-kappa B p65 compared with WT cells. Transfection of LGALS3(-/-) macrophages with NLRP3 small interfering RNA attenuated production in response to palmitate and LPS plus palmitate. Obtained results suggest important protective roles for Gal-3 in obesity-induced inflammation and diabetes.
T2  - Diabetes
T1  - Galectin-3 Deficiency Accelerates High-Fat Diet-Induced Obesity and Amplifies Inflammation in Adipose Tissue and Pancreatic Islets
IS  - 6
VL  - 62
DO  - 10.2337/db12-0222
SP  - 131
EP  - 1944
ER  - 

@article{
author = "Pejnović, Nada N and Pantić, Jelena M and Jovanović, Ivan P and Radosavljević, Gordana D and Milovanović, Marija Z and Nikolić, Ivana and Zdravković, Nemanja S and Đukić, Aleksandar Lj and Arsenijević, Nebojsa N and Lukić, Miodrag L",
year = "2013",
abstract = "Obesity-induced diabetes is associated with low-grade inflammation in adipose tissue and macrophage infiltration of islets. We show that ablation of galectin-3 (Gal-3), a galactoside-binding lectin, accelerates high-fat diet-induced obesity and diabetes. Obese LGALS3(-/-) mice have increased body weight, amount of total visceral adipose tissue (VAT), fasting blood glucose and insulin levels, homeostasis model assessment of insulin resistance, and markers of systemic inflammation compared with diet-matched wild-type (WT) animals. VAT of obese LGALS3(-/-) mice exhibited increased incidence of type 1 T and NKT lymphocytes and proinflammatory CD11c(+)CD11b(+) macrophages and decreased CD4(+)CD25(+)FoxP3(+) regulatory T cells and M2 macrophages. Pronounced mononuclear cell infiltrate, increased expression of NLRP3 inflammasome and interleukin-1 beta (IL-1 beta) in macrophages, and increased accumulation of advanced glycation end products (AGEs) and receptor for AGE (RAGE) expression were present in pancreatic islets of obese LGALS3(-/-) animals accompanied with elevated phosphorylated nuclear factor-kappa B (NF-kappa B) p65 and mature caspase-1 protein expression in pancreatic tissue and VAT. In vitro stimulation of LGALS3(-/-) peritoneal macrophages with lipopolysaccharide (LPS) and saturated fatty acid palmitate caused increased caspase-l-dependent IL-1 beta production and increased phosphorylation of NF-kappa B p65 compared with WT cells. Transfection of LGALS3(-/-) macrophages with NLRP3 small interfering RNA attenuated production in response to palmitate and LPS plus palmitate. Obtained results suggest important protective roles for Gal-3 in obesity-induced inflammation and diabetes.",
journal = "Diabetes",
title = "Galectin-3 Deficiency Accelerates High-Fat Diet-Induced Obesity and Amplifies Inflammation in Adipose Tissue and Pancreatic Islets",
number = "6",
volume = "62",
doi = "10.2337/db12-0222",
pages = "131-1944"
}

Pejnović, N. N., Pantić, J. M., Jovanović, I. P., Radosavljević, G. D., Milovanović, M. Z., Nikolić, I., Zdravković, N. S., Đukić, A. L., Arsenijević, N. N.,& Lukić, M. L.. (2013). Galectin-3 Deficiency Accelerates High-Fat Diet-Induced Obesity and Amplifies Inflammation in Adipose Tissue and Pancreatic Islets. in Diabetes, 62(6), 131-1944.
https://doi.org/10.2337/db12-0222

Pejnović NN, Pantić JM, Jovanović IP, Radosavljević GD, Milovanović MZ, Nikolić I, Zdravković NS, Đukić AL, Arsenijević NN, Lukić ML. Galectin-3 Deficiency Accelerates High-Fat Diet-Induced Obesity and Amplifies Inflammation in Adipose Tissue and Pancreatic Islets. in Diabetes. 2013;62(6):131-1944.
doi:10.2337/db12-0222 .

Pejnović, Nada N, Pantić, Jelena M, Jovanović, Ivan P, Radosavljević, Gordana D, Milovanović, Marija Z, Nikolić, Ivana, Zdravković, Nemanja S, Đukić, Aleksandar Lj, Arsenijević, Nebojsa N, Lukić, Miodrag L, "Galectin-3 Deficiency Accelerates High-Fat Diet-Induced Obesity and Amplifies Inflammation in Adipose Tissue and Pancreatic Islets" in Diabetes, 62, no. 6 (2013):131-1944,
https://doi.org/10.2337/db12-0222 . .

TY  - CONF
AU  - Nikolić, Ivana
AU  - Saksida, Tamara
AU  - Stojanović, Ivana D.
AU  - Lukić, Miodrag L
AU  - Stošić-Grujičić, Stanislava
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1115
C3  - Immunology
T1  - Galectin-3 deficiency preserves pancreatic islets function in basal conditions and under cytotoxic stimuli
IS  - null
VL  - 137
SP  - 359
EP  - 540
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1115
ER  - 

@conference{
author = "Nikolić, Ivana and Saksida, Tamara and Stojanović, Ivana D. and Lukić, Miodrag L and Stošić-Grujičić, Stanislava",
year = "2012",
journal = "Immunology",
title = "Galectin-3 deficiency preserves pancreatic islets function in basal conditions and under cytotoxic stimuli",
number = "null",
volume = "137",
pages = "359-540",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1115"
}

Nikolić, I., Saksida, T., Stojanović, I. D., Lukić, M. L.,& Stošić-Grujičić, S.. (2012). Galectin-3 deficiency preserves pancreatic islets function in basal conditions and under cytotoxic stimuli. in Immunology, 137(null), 359-540.
https://hdl.handle.net/21.15107/rcub_ibiss_1115

Nikolić I, Saksida T, Stojanović ID, Lukić ML, Stošić-Grujičić S. Galectin-3 deficiency preserves pancreatic islets function in basal conditions and under cytotoxic stimuli. in Immunology. 2012;137(null):359-540.
https://hdl.handle.net/21.15107/rcub_ibiss_1115 .

Nikolić, Ivana, Saksida, Tamara, Stojanović, Ivana D., Lukić, Miodrag L, Stošić-Grujičić, Stanislava, "Galectin-3 deficiency preserves pancreatic islets function in basal conditions and under cytotoxic stimuli" in Immunology, 137, no. null (2012):359-540,
https://hdl.handle.net/21.15107/rcub_ibiss_1115 .

TY  - JOUR
AU  - Stojanović, Ivana D.
AU  - Saksida, Tamara
AU  - Nikolić, Ivana
AU  - Nicoletti, Ferdinando
AU  - Stošić-Grujičić, Stanislava
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1155
AB  - During pathogenesis of diabetes, pancreatic islets are exposed to high levels of cytokines and other inflammatory mediators that induce deterioration of insulin-producing beta cells. Macrophage migration inhibitory factor (MIF) plays a key role in the onset and development of several immunoinflammatory diseases and also controls apoptotic cell death. Because the occurrence of apoptosis plays a pathogenetic role in beta cell death during type 1 diabetes development and MIF is expressed in beta cells, we explored the influence of MIF deficiency on cytokine-induced apoptosis in pancreatic islets. The results indicated clearly that elevated MIF secretion preceded C57BL/6 pancreatic islets death induced by interferon (IFN)-? + tumour necrosis factor (TNF)-a + interleukin (IL)-1 beta. Consequently, MIF-deficient [MIF-knock-out (KO)] pancreatic islets or islet cells showed significant resistance to cytokine-induced death than those isolated from C57BL/6 mice. Furthermore, upon exposure to cytokines pancreatic islets from MIF-KO mice maintained normal insulin expression and produced less cyclooxygenase-2 (COX-2) than those from wild-type C57BL6 mice. The final outcome of cytokine-induced islet apoptosis in islets from wild-type mice was the activation of mitochondrial membrane pore-forming protein Bcl-2-associated X protein and effector caspase 3. In contrast, these apoptotic mediators remained at normal levels in islets from MIF-KO mice suggesting that MIF absence prevented initiation of the mitochondrial apoptotic pathway. Additionally, the protection from apoptosis was also mediated by up-regulation of prosurvival kinase extracellular-regulated kinase 1/2 in MIF-KO islets. These data indicate that MIF is involved in the propagation of pancreatic islets apoptosis probably via nuclear factor-?B and mitochondria-related proteins.
T2  - Clinical and Experimental Immunology
T1  - Macrophage migration inhibitory factor deficiency protects pancreatic islets from cytokine-induced apoptosis in vitro
IS  - 2
VL  - 169
SP  - 365
EP  - 163
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1155
ER  - 

@article{
author = "Stojanović, Ivana D. and Saksida, Tamara and Nikolić, Ivana and Nicoletti, Ferdinando and Stošić-Grujičić, Stanislava",
year = "2012",
abstract = "During pathogenesis of diabetes, pancreatic islets are exposed to high levels of cytokines and other inflammatory mediators that induce deterioration of insulin-producing beta cells. Macrophage migration inhibitory factor (MIF) plays a key role in the onset and development of several immunoinflammatory diseases and also controls apoptotic cell death. Because the occurrence of apoptosis plays a pathogenetic role in beta cell death during type 1 diabetes development and MIF is expressed in beta cells, we explored the influence of MIF deficiency on cytokine-induced apoptosis in pancreatic islets. The results indicated clearly that elevated MIF secretion preceded C57BL/6 pancreatic islets death induced by interferon (IFN)-? + tumour necrosis factor (TNF)-a + interleukin (IL)-1 beta. Consequently, MIF-deficient [MIF-knock-out (KO)] pancreatic islets or islet cells showed significant resistance to cytokine-induced death than those isolated from C57BL/6 mice. Furthermore, upon exposure to cytokines pancreatic islets from MIF-KO mice maintained normal insulin expression and produced less cyclooxygenase-2 (COX-2) than those from wild-type C57BL6 mice. The final outcome of cytokine-induced islet apoptosis in islets from wild-type mice was the activation of mitochondrial membrane pore-forming protein Bcl-2-associated X protein and effector caspase 3. In contrast, these apoptotic mediators remained at normal levels in islets from MIF-KO mice suggesting that MIF absence prevented initiation of the mitochondrial apoptotic pathway. Additionally, the protection from apoptosis was also mediated by up-regulation of prosurvival kinase extracellular-regulated kinase 1/2 in MIF-KO islets. These data indicate that MIF is involved in the propagation of pancreatic islets apoptosis probably via nuclear factor-?B and mitochondria-related proteins.",
journal = "Clinical and Experimental Immunology",
title = "Macrophage migration inhibitory factor deficiency protects pancreatic islets from cytokine-induced apoptosis in vitro",
number = "2",
volume = "169",
pages = "365-163",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1155"
}

Stojanović, I. D., Saksida, T., Nikolić, I., Nicoletti, F.,& Stošić-Grujičić, S.. (2012). Macrophage migration inhibitory factor deficiency protects pancreatic islets from cytokine-induced apoptosis in vitro. in Clinical and Experimental Immunology, 169(2), 365-163.
https://hdl.handle.net/21.15107/rcub_ibiss_1155

Stojanović ID, Saksida T, Nikolić I, Nicoletti F, Stošić-Grujičić S. Macrophage migration inhibitory factor deficiency protects pancreatic islets from cytokine-induced apoptosis in vitro. in Clinical and Experimental Immunology. 2012;169(2):365-163.
https://hdl.handle.net/21.15107/rcub_ibiss_1155 .

Stojanović, Ivana D., Saksida, Tamara, Nikolić, Ivana, Nicoletti, Ferdinando, Stošić-Grujičić, Stanislava, "Macrophage migration inhibitory factor deficiency protects pancreatic islets from cytokine-induced apoptosis in vitro" in Clinical and Experimental Immunology, 169, no. 2 (2012):365-163,
https://hdl.handle.net/21.15107/rcub_ibiss_1155 .

TY  - CONF
AU  - Šipetić-Grujicić, Sandra B
AU  - Nikolić, Ivana
AU  - Stojanović, Ivana D.
AU  - Saksida, Tamara
AU  - Nicoletti, Ferdinando
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1116
C3  - Immunology
T1  - A novel carbon monoxide-releasing molecule ALF421 attenuates the development of autoimmune diabetes in mice induced by multiple low doses of streptozotocin
IS  - null
VL  - 137
SP  - 113
EP  - 654
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1116
ER  - 

@conference{
author = "Šipetić-Grujicić, Sandra B and Nikolić, Ivana and Stojanović, Ivana D. and Saksida, Tamara and Nicoletti, Ferdinando",
year = "2012",
journal = "Immunology",
title = "A novel carbon monoxide-releasing molecule ALF421 attenuates the development of autoimmune diabetes in mice induced by multiple low doses of streptozotocin",
number = "null",
volume = "137",
pages = "113-654",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1116"
}

Šipetić-Grujicić, S. B., Nikolić, I., Stojanović, I. D., Saksida, T.,& Nicoletti, F.. (2012). A novel carbon monoxide-releasing molecule ALF421 attenuates the development of autoimmune diabetes in mice induced by multiple low doses of streptozotocin. in Immunology, 137(null), 113-654.
https://hdl.handle.net/21.15107/rcub_ibiss_1116

Šipetić-Grujicić SB, Nikolić I, Stojanović ID, Saksida T, Nicoletti F. A novel carbon monoxide-releasing molecule ALF421 attenuates the development of autoimmune diabetes in mice induced by multiple low doses of streptozotocin. in Immunology. 2012;137(null):113-654.
https://hdl.handle.net/21.15107/rcub_ibiss_1116 .

Šipetić-Grujicić, Sandra B, Nikolić, Ivana, Stojanović, Ivana D., Saksida, Tamara, Nicoletti, Ferdinando, "A novel carbon monoxide-releasing molecule ALF421 attenuates the development of autoimmune diabetes in mice induced by multiple low doses of streptozotocin" in Immunology, 137, no. null (2012):113-654,
https://hdl.handle.net/21.15107/rcub_ibiss_1116 .

TY  - JOUR
AU  - Poljarević, Jelena M
AU  - Sabo, Tibor J
AU  - Grgurić-Sipka, Sanja R
AU  - Stošić-Grujičić, Stanislava
AU  - Saksida, Tamara
AU  - Blaževski, Jana
AU  - Petković, Filip
AU  - Miljković, Đorđe
AU  - Nikolić, Ivana
AU  - Momčilović, Miljana
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1233
AB  - We have recently reported that a novel octahedral Pt(IV) complex with di-n-propyl-(S,S)-ethylenediamine-N,N'-di-2-(3-cyclohexyl)propanoato ligand has a potent cytotoxic effect on glioma, melanoma and fibrosarcoma cell lines. In this work, we investigated the influence of the Pt(IV) compound on immune cells. We determined its effect on the viability of spleen cells and lymph node cells and on their capability to produce interferon (IFN)-gamma and interleukin (IL)-17. Also, we researched the compound's impact on peritoneal macrophages and generation of NO in these cells. Our results show that the complex has limited influence on cell viability of immune cells, but profound inhibitory effect on the production of examined immune mediators. These results are valuable as they show that the novel Pt(IV) complex applied in concentrations which are effective against tumor cells do not affect immune cell viability. Moreover, they also imply that the complex has immunomodulatory properties. (C) 2011 Elsevier Masson SAS. All rights reserved.
T2  - European Journal of Medicinal Chemistry
T1  - Novel octahedral Pt(IV) complex with di-n-propyl-(S,S)-ethylenediamine-N,N '-di-2-(3-cyclohexyl)propanoato ligand exerts potent immunomodulatory effects
VL  - 47
EP  - 201
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1233
ER  - 

@article{
author = "Poljarević, Jelena M and Sabo, Tibor J and Grgurić-Sipka, Sanja R and Stošić-Grujičić, Stanislava and Saksida, Tamara and Blaževski, Jana and Petković, Filip and Miljković, Đorđe and Nikolić, Ivana and Momčilović, Miljana",
year = "2012",
abstract = "We have recently reported that a novel octahedral Pt(IV) complex with di-n-propyl-(S,S)-ethylenediamine-N,N'-di-2-(3-cyclohexyl)propanoato ligand has a potent cytotoxic effect on glioma, melanoma and fibrosarcoma cell lines. In this work, we investigated the influence of the Pt(IV) compound on immune cells. We determined its effect on the viability of spleen cells and lymph node cells and on their capability to produce interferon (IFN)-gamma and interleukin (IL)-17. Also, we researched the compound's impact on peritoneal macrophages and generation of NO in these cells. Our results show that the complex has limited influence on cell viability of immune cells, but profound inhibitory effect on the production of examined immune mediators. These results are valuable as they show that the novel Pt(IV) complex applied in concentrations which are effective against tumor cells do not affect immune cell viability. Moreover, they also imply that the complex has immunomodulatory properties. (C) 2011 Elsevier Masson SAS. All rights reserved.",
journal = "European Journal of Medicinal Chemistry",
title = "Novel octahedral Pt(IV) complex with di-n-propyl-(S,S)-ethylenediamine-N,N '-di-2-(3-cyclohexyl)propanoato ligand exerts potent immunomodulatory effects",
volume = "47",
pages = "201",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1233"
}

Poljarević, J. M., Sabo, T. J., Grgurić-Sipka, S. R., Stošić-Grujičić, S., Saksida, T., Blaževski, J., Petković, F., Miljković, Đ., Nikolić, I.,& Momčilović, M.. (2012). Novel octahedral Pt(IV) complex with di-n-propyl-(S,S)-ethylenediamine-N,N '-di-2-(3-cyclohexyl)propanoato ligand exerts potent immunomodulatory effects. in European Journal of Medicinal Chemistry, 47.
https://hdl.handle.net/21.15107/rcub_ibiss_1233

Poljarević JM, Sabo TJ, Grgurić-Sipka SR, Stošić-Grujičić S, Saksida T, Blaževski J, Petković F, Miljković Đ, Nikolić I, Momčilović M. Novel octahedral Pt(IV) complex with di-n-propyl-(S,S)-ethylenediamine-N,N '-di-2-(3-cyclohexyl)propanoato ligand exerts potent immunomodulatory effects. in European Journal of Medicinal Chemistry. 2012;47:null-201.
https://hdl.handle.net/21.15107/rcub_ibiss_1233 .

Poljarević, Jelena M, Sabo, Tibor J, Grgurić-Sipka, Sanja R, Stošić-Grujičić, Stanislava, Saksida, Tamara, Blaževski, Jana, Petković, Filip, Miljković, Đorđe, Nikolić, Ivana, Momčilović, Miljana, "Novel octahedral Pt(IV) complex with di-n-propyl-(S,S)-ethylenediamine-N,N '-di-2-(3-cyclohexyl)propanoato ligand exerts potent immunomodulatory effects" in European Journal of Medicinal Chemistry, 47 (2012),
https://hdl.handle.net/21.15107/rcub_ibiss_1233 .

TY  - CONF
AU  - Nikolić, Ivana
AU  - Saksida, Tamara
AU  - Zdravković, N
AU  - Stojanović, Ivana D.
AU  - Lukić, Miodrag L
AU  - Stošić-Grujičić, Stanislava
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1106
C3  - Diabetologia
T1  - Galectin-3 deficiency confers resistance to cytokine-induced apoptosis of pancreatic islets - role of mitochondrial pathway
IS  - null
VL  - 55
SP  - 167
EP  - S208
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1106
ER  - 

@conference{
author = "Nikolić, Ivana and Saksida, Tamara and Zdravković, N and Stojanović, Ivana D. and Lukić, Miodrag L and Stošić-Grujičić, Stanislava",
year = "2012",
journal = "Diabetologia",
title = "Galectin-3 deficiency confers resistance to cytokine-induced apoptosis of pancreatic islets - role of mitochondrial pathway",
number = "null",
volume = "55",
pages = "167-S208",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1106"
}

Nikolić, I., Saksida, T., Zdravković, N., Stojanović, I. D., Lukić, M. L.,& Stošić-Grujičić, S.. (2012). Galectin-3 deficiency confers resistance to cytokine-induced apoptosis of pancreatic islets - role of mitochondrial pathway. in Diabetologia, 55(null), 167-S208.
https://hdl.handle.net/21.15107/rcub_ibiss_1106

Nikolić I, Saksida T, Zdravković N, Stojanović ID, Lukić ML, Stošić-Grujičić S. Galectin-3 deficiency confers resistance to cytokine-induced apoptosis of pancreatic islets - role of mitochondrial pathway. in Diabetologia. 2012;55(null):167-S208.
https://hdl.handle.net/21.15107/rcub_ibiss_1106 .

Nikolić, Ivana, Saksida, Tamara, Zdravković, N, Stojanović, Ivana D., Lukić, Miodrag L, Stošić-Grujičić, Stanislava, "Galectin-3 deficiency confers resistance to cytokine-induced apoptosis of pancreatic islets - role of mitochondrial pathway" in Diabetologia, 55, no. null (2012):167-S208,
https://hdl.handle.net/21.15107/rcub_ibiss_1106 .

TY  - CONF
AU  - Stojanović, Ivana D.
AU  - Nikolić, Ivana
AU  - Saksida, Tamara
AU  - Vujičić, Milica
AU  - Stošić-Grujičić, Stanislava
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1107
C3  - Diabetologia
T1  - The role of glucocorticoids in glucose intolerance development in MIF-deficient mice
IS  - null
VL  - 55
SP  - 57
EP  - S266
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1107
ER  - 

@conference{
author = "Stojanović, Ivana D. and Nikolić, Ivana and Saksida, Tamara and Vujičić, Milica and Stošić-Grujičić, Stanislava",
year = "2012",
journal = "Diabetologia",
title = "The role of glucocorticoids in glucose intolerance development in MIF-deficient mice",
number = "null",
volume = "55",
pages = "57-S266",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1107"
}

Stojanović, I. D., Nikolić, I., Saksida, T., Vujičić, M.,& Stošić-Grujičić, S.. (2012). The role of glucocorticoids in glucose intolerance development in MIF-deficient mice. in Diabetologia, 55(null), 57-S266.
https://hdl.handle.net/21.15107/rcub_ibiss_1107

Stojanović ID, Nikolić I, Saksida T, Vujičić M, Stošić-Grujičić S. The role of glucocorticoids in glucose intolerance development in MIF-deficient mice. in Diabetologia. 2012;55(null):57-S266.
https://hdl.handle.net/21.15107/rcub_ibiss_1107 .

Stojanović, Ivana D., Nikolić, Ivana, Saksida, Tamara, Vujičić, Milica, Stošić-Grujičić, Stanislava, "The role of glucocorticoids in glucose intolerance development in MIF-deficient mice" in Diabetologia, 55, no. null (2012):57-S266,
https://hdl.handle.net/21.15107/rcub_ibiss_1107 .