TY  - JOUR
AU  - Jovičić, Nemanja
AU  - Petrović, Ivica
AU  - Pejnović, Nada
AU  - Ljujić, Biljana
AU  - Miletić Kovačević, Marina
AU  - Pavlović, Slađana
AU  - Jeftić, Ilija
AU  - Đukić, Aleksandar
AU  - Srejović, Ivan
AU  - Jakovljević, Vladimir
AU  - Lukić, Miodrag L.
PY  - 2021
UR  - https://www.frontiersin.org/articles/10.3389/fphar.2021.714683/full
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/4697
AB  - Galectin-3 (Gal-3) has diverse roles in inflammatory and autoimmune diseases. There is evidence that Gal-3 plays a role in both type 1 and type 2 diabetes. While the role of Gal-3 expression in immune cells invading the pancreatic islets in the experimental model of type 1 diabetes mellitus has been already studied, the importance of the overexpression of Gal-3 in the target β cells is not defined. Therefore, we used multiple low doses of streptozotocin (MLD-STZ)-induced diabetes in C57Bl/6 mice to analyze the effect of transgenic (TG) overexpression of Gal-3 in β cells. Our results demonstrated that the overexpression of Gal-3 protected β cells from apoptosis and attenuated MLD-STZ-induced hyperglycemia, glycosuria, and ketonuria. The cellular analysis of pancreata and draining lymph nodes showed that Gal-3 overexpression significantly decreased the number of pro-inflammatory cells without affecting the presence of T-regulatory cells. As the application of exogenous interleukin 33 (IL-33) given from the beginning of MLD-STZ diabetes induction attenuates the development of disease, by increasing the presence of regulatory FoxP3+ ST2+ cells, we evaluated the potential synergistic effect of the exogenous IL-33 and TG overexpression of Gal-3 in β cells at the later stage of diabetogenesis. The addition of IL-33 potentiated the survival of β cells and attenuated diabetes even when administered later, after the onset of hyperglycemia (12-18 days), suggesting that protection from apoptosis and immunoregulation by IL-33 may attenuate type 1 diabetes.
PB  - Lausanne: Frontiers Media S.A.
T2  - Frontiers in Pharmacology
T1  - Transgenic Overexpression of Galectin-3 in Pancreatic β Cells Attenuates Hyperglycemia in Mice: Synergistic Antidiabetic Effect With Exogenous IL-33.
VL  - 12
DO  - 10.3389/fphar.2021.714683
SP  - 714683
ER  - 

@article{
author = "Jovičić, Nemanja and Petrović, Ivica and Pejnović, Nada and Ljujić, Biljana and Miletić Kovačević, Marina and Pavlović, Slađana and Jeftić, Ilija and Đukić, Aleksandar and Srejović, Ivan and Jakovljević, Vladimir and Lukić, Miodrag L.",
year = "2021",
abstract = "Galectin-3 (Gal-3) has diverse roles in inflammatory and autoimmune diseases. There is evidence that Gal-3 plays a role in both type 1 and type 2 diabetes. While the role of Gal-3 expression in immune cells invading the pancreatic islets in the experimental model of type 1 diabetes mellitus has been already studied, the importance of the overexpression of Gal-3 in the target β cells is not defined. Therefore, we used multiple low doses of streptozotocin (MLD-STZ)-induced diabetes in C57Bl/6 mice to analyze the effect of transgenic (TG) overexpression of Gal-3 in β cells. Our results demonstrated that the overexpression of Gal-3 protected β cells from apoptosis and attenuated MLD-STZ-induced hyperglycemia, glycosuria, and ketonuria. The cellular analysis of pancreata and draining lymph nodes showed that Gal-3 overexpression significantly decreased the number of pro-inflammatory cells without affecting the presence of T-regulatory cells. As the application of exogenous interleukin 33 (IL-33) given from the beginning of MLD-STZ diabetes induction attenuates the development of disease, by increasing the presence of regulatory FoxP3+ ST2+ cells, we evaluated the potential synergistic effect of the exogenous IL-33 and TG overexpression of Gal-3 in β cells at the later stage of diabetogenesis. The addition of IL-33 potentiated the survival of β cells and attenuated diabetes even when administered later, after the onset of hyperglycemia (12-18 days), suggesting that protection from apoptosis and immunoregulation by IL-33 may attenuate type 1 diabetes.",
publisher = "Lausanne: Frontiers Media S.A.",
journal = "Frontiers in Pharmacology",
title = "Transgenic Overexpression of Galectin-3 in Pancreatic β Cells Attenuates Hyperglycemia in Mice: Synergistic Antidiabetic Effect With Exogenous IL-33.",
volume = "12",
doi = "10.3389/fphar.2021.714683",
pages = "714683"
}

Jovičić, N., Petrović, I., Pejnović, N., Ljujić, B., Miletić Kovačević, M., Pavlović, S., Jeftić, I., Đukić, A., Srejović, I., Jakovljević, V.,& Lukić, M. L.. (2021). Transgenic Overexpression of Galectin-3 in Pancreatic β Cells Attenuates Hyperglycemia in Mice: Synergistic Antidiabetic Effect With Exogenous IL-33.. in Frontiers in Pharmacology
Lausanne: Frontiers Media S.A.., 12, 714683.
https://doi.org/10.3389/fphar.2021.714683

Jovičić N, Petrović I, Pejnović N, Ljujić B, Miletić Kovačević M, Pavlović S, Jeftić I, Đukić A, Srejović I, Jakovljević V, Lukić ML. Transgenic Overexpression of Galectin-3 in Pancreatic β Cells Attenuates Hyperglycemia in Mice: Synergistic Antidiabetic Effect With Exogenous IL-33.. in Frontiers in Pharmacology. 2021;12:714683.
doi:10.3389/fphar.2021.714683 .

Jovičić, Nemanja, Petrović, Ivica, Pejnović, Nada, Ljujić, Biljana, Miletić Kovačević, Marina, Pavlović, Slađana, Jeftić, Ilija, Đukić, Aleksandar, Srejović, Ivan, Jakovljević, Vladimir, Lukić, Miodrag L., "Transgenic Overexpression of Galectin-3 in Pancreatic β Cells Attenuates Hyperglycemia in Mice: Synergistic Antidiabetic Effect With Exogenous IL-33." in Frontiers in Pharmacology, 12 (2021):714683,
https://doi.org/10.3389/fphar.2021.714683 . .

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  - 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  - 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  - Stošić-Grujičić, Stanislava
AU  - Maksimović-Ivanić, Danijela
AU  - Miljković, Đorđe
AU  - Trajković, Vladimir S
AU  - Lukić, Miodrag L
AU  - Mostarica-Stojković, Marija B
PY  - 2002
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1786
PB  - Elsevier
C3  - Transplantation Proceedings
T1  - Inhibition of autoimmune diabetes by mycophenolate mofetil is associated with down-regulation of Th1 cytokine-induced apoptosis in the target tissue
IS  - 7
VL  - 34
DO  - 10.1016/S0041-1345(02)03502-9
SP  - 2955
EP  - 2957
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1786
ER  - 

@conference{
author = "Stošić-Grujičić, Stanislava and Maksimović-Ivanić, Danijela and Miljković, Đorđe and Trajković, Vladimir S and Lukić, Miodrag L and Mostarica-Stojković, Marija B",
year = "2002",
publisher = "Elsevier",
journal = "Transplantation Proceedings",
title = "Inhibition of autoimmune diabetes by mycophenolate mofetil is associated with down-regulation of Th1 cytokine-induced apoptosis in the target tissue",
number = "7",
volume = "34",
doi = "10.1016/S0041-1345(02)03502-9",
pages = "2955-2957",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1786"
}

Stošić-Grujičić, S., Maksimović-Ivanić, D., Miljković, Đ., Trajković, V. S., Lukić, M. L.,& Mostarica-Stojković, M. B.. (2002). Inhibition of autoimmune diabetes by mycophenolate mofetil is associated with down-regulation of Th1 cytokine-induced apoptosis in the target tissue. in Transplantation Proceedings
Elsevier., 34(7), 2955-2957.
https://doi.org/10.1016/S0041-1345(02)03502-9
https://hdl.handle.net/21.15107/rcub_ibiss_1786

Stošić-Grujičić S, Maksimović-Ivanić D, Miljković Đ, Trajković VS, Lukić ML, Mostarica-Stojković MB. Inhibition of autoimmune diabetes by mycophenolate mofetil is associated with down-regulation of Th1 cytokine-induced apoptosis in the target tissue. in Transplantation Proceedings. 2002;34(7):2955-2957.
doi:10.1016/S0041-1345(02)03502-9
https://hdl.handle.net/21.15107/rcub_ibiss_1786 .

Stošić-Grujičić, Stanislava, Maksimović-Ivanić, Danijela, Miljković, Đorđe, Trajković, Vladimir S, Lukić, Miodrag L, Mostarica-Stojković, Marija B, "Inhibition of autoimmune diabetes by mycophenolate mofetil is associated with down-regulation of Th1 cytokine-induced apoptosis in the target tissue" in Transplantation Proceedings, 34, no. 7 (2002):2955-2957,
https://doi.org/10.1016/S0041-1345(02)03502-9 .,
https://hdl.handle.net/21.15107/rcub_ibiss_1786 .

TY  - JOUR
AU  - Stošić-Grujičić, Stanislava
AU  - Maksimović-Ivanić, Danijela
AU  - Badovinac, Vladimir
AU  - Samardžić, Tatjana S.
AU  - Trajković, Vladimir S
AU  - Lukić, Miodrag L
AU  - Mostarica-Stojković, Marija B
PY  - 2001
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1821
AB  - We have shown recently that xanthine derivative pentoxifylline (PTX) downregulates an inflammatory autoimmune process triggered in genetically susceptible Dark Agouti rats by multiple low doses of streptozotocin (MLD-SZ, 20 mg/kg/day ip for 5 days). We studied the cellular and molecular consequences of PTX treatment during MLD-SZ-induced diabetes with special emphasis on local vs. systemic production of inflammatory mediators. Administration of PTX (200 mg/kg/day for 10 days) during induction of the disease reduced clinical signs of diabetes and protected rats from development of destructive intrainsulitis. Pentoxifylline did not affect diabetogenic effect of single high dose of SZ (100 mg/kg SZ). Ex vivo analysis of the islets of Langerhans performed in early disease development revealed that PTX downregulates production of proinflammatory cytokines IFN-gamma and TNF, as well as inducible nitric oxide synthase (iNOS) expression and NO production. In addition, PTX treatment suppressed splenocyte autoreactivity, as well as the frequency of cells expressing IL-2R and MHC class II antigens. There was no evidence of any changes in proportion of ICAM-1 and LFA-1 expressing splenocytes in comparison to control MLD-SZ-treated animals. In contrast to suppressed intraislet production, high peripheral expression of both iNOS mRNA and NO was found in MLD-SZ rats treated with PTX. Taken together, the data indicate that the effect on both systemic and intra-islet production of NO, suppression of autoreactive cell activation and of local type 1 cytokine release may contribute to the therapeutic benefit achieved by PTX in the rat. (C) 2001 Academic Press.
T2  - Journal of Autoimmunity
T1  - Antidiabetogenic effect of pentoxifylline is associated with systemic and target tissue modulation of cytokines and nitric oxide production
IS  - 1
VL  - 16
EP  - 58
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1821
ER  - 

@article{
author = "Stošić-Grujičić, Stanislava and Maksimović-Ivanić, Danijela and Badovinac, Vladimir and Samardžić, Tatjana S. and Trajković, Vladimir S and Lukić, Miodrag L and Mostarica-Stojković, Marija B",
year = "2001",
abstract = "We have shown recently that xanthine derivative pentoxifylline (PTX) downregulates an inflammatory autoimmune process triggered in genetically susceptible Dark Agouti rats by multiple low doses of streptozotocin (MLD-SZ, 20 mg/kg/day ip for 5 days). We studied the cellular and molecular consequences of PTX treatment during MLD-SZ-induced diabetes with special emphasis on local vs. systemic production of inflammatory mediators. Administration of PTX (200 mg/kg/day for 10 days) during induction of the disease reduced clinical signs of diabetes and protected rats from development of destructive intrainsulitis. Pentoxifylline did not affect diabetogenic effect of single high dose of SZ (100 mg/kg SZ). Ex vivo analysis of the islets of Langerhans performed in early disease development revealed that PTX downregulates production of proinflammatory cytokines IFN-gamma and TNF, as well as inducible nitric oxide synthase (iNOS) expression and NO production. In addition, PTX treatment suppressed splenocyte autoreactivity, as well as the frequency of cells expressing IL-2R and MHC class II antigens. There was no evidence of any changes in proportion of ICAM-1 and LFA-1 expressing splenocytes in comparison to control MLD-SZ-treated animals. In contrast to suppressed intraislet production, high peripheral expression of both iNOS mRNA and NO was found in MLD-SZ rats treated with PTX. Taken together, the data indicate that the effect on both systemic and intra-islet production of NO, suppression of autoreactive cell activation and of local type 1 cytokine release may contribute to the therapeutic benefit achieved by PTX in the rat. (C) 2001 Academic Press.",
journal = "Journal of Autoimmunity",
title = "Antidiabetogenic effect of pentoxifylline is associated with systemic and target tissue modulation of cytokines and nitric oxide production",
number = "1",
volume = "16",
pages = "58",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1821"
}

Stošić-Grujičić, S., Maksimović-Ivanić, D., Badovinac, V., Samardžić, T. S., Trajković, V. S., Lukić, M. L.,& Mostarica-Stojković, M. B.. (2001). Antidiabetogenic effect of pentoxifylline is associated with systemic and target tissue modulation of cytokines and nitric oxide production. in Journal of Autoimmunity, 16(1).
https://hdl.handle.net/21.15107/rcub_ibiss_1821

Stošić-Grujičić S, Maksimović-Ivanić D, Badovinac V, Samardžić TS, Trajković VS, Lukić ML, Mostarica-Stojković MB. Antidiabetogenic effect of pentoxifylline is associated with systemic and target tissue modulation of cytokines and nitric oxide production. in Journal of Autoimmunity. 2001;16(1):null-58.
https://hdl.handle.net/21.15107/rcub_ibiss_1821 .

Stošić-Grujičić, Stanislava, Maksimović-Ivanić, Danijela, Badovinac, Vladimir, Samardžić, Tatjana S., Trajković, Vladimir S, Lukić, Miodrag L, Mostarica-Stojković, Marija B, "Antidiabetogenic effect of pentoxifylline is associated with systemic and target tissue modulation of cytokines and nitric oxide production" in Journal of Autoimmunity, 16, no. 1 (2001),
https://hdl.handle.net/21.15107/rcub_ibiss_1821 .