TY  - JOUR
AU  - Stančić, Ana
AU  - Saksida, Tamara
AU  - Markelić, Milica
AU  - Vučetić, Milica
AU  - Grigorov, Ilijana
AU  - Martinović, Vesna
AU  - Mićanović, Dragica
AU  - Ivanović, Anđelija
AU  - Veličković, Ksenija
AU  - Savić, Nevena
AU  - Otašević, Vesna
PY  - 2022
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/4910
AB  - The main pathological hallmark of diabetes is the loss of functional β-cells. Among several types of β-cell death in diabetes, the
involvement of ferroptosis remains elusive. Therefore, we investigated the potential of diabetes-mimicking factors: high glucose
(HG), proinflammatory cytokines, hydrogen peroxide (H2O2), or diabetogenic agent streptozotocin (STZ) to induce ferroptosis
of β-cells in vitro. Furthermore, we tested the contribution of ferroptosis to injury of pancreatic islets in an STZ-induced
in vivo diabetic model. All in vitro treatments increased loss of Rin-5F cells along with the accumulation of reactive oxygen
species, lipid peroxides and iron, inactivation of NF-E2-related factor 2 (Nrf2), and decrease in glutathione peroxidase 4
expression and mitochondrial membrane potential (MMP). Ferrostatin 1 (Fer-1), ferroptosis inhibitor, diminished the abovestated effects and rescued cells from death in case of HG, STZ, and H2O2 treatments, while failed to increase MMP and to
attenuate cell death after the cytokines’ treatment. Moreover, Fer-1 protected pancreatic islets from STZ-induced injury in
diabetic in vivo model, since it decreased infiltration of macrophages and accumulation of lipid peroxides and increased the
population of insulin-positive cells. Such results revealed differences between diabetogenic stimuli in determining the destiny of
β-cells, emerging HG, H2O2, and STZ, but not cytokines, as contributing factors to ferroptosis and shed new light on an
antidiabetic strategy based on Nrf2 activation. Thus, targeting ferroptosis in diabetes might be a promising new approach for
preservation of the β-cell population. Our results obtained from in vivo study strongly justify this approach.
PB  - London:Hindawi
T2  - Oxidative Medicine and Cellular Longevity
T1  - Ferroptosis as a Novel Determinant of β-Cell Death in Diabetic Conditions
VL  - 2022
DO  - 10.1155/2022/3873420
SP  - 3873420
ER  - 

@article{
author = "Stančić, Ana and Saksida, Tamara and Markelić, Milica and Vučetić, Milica and Grigorov, Ilijana and Martinović, Vesna and Mićanović, Dragica and Ivanović, Anđelija and Veličković, Ksenija and Savić, Nevena and Otašević, Vesna",
year = "2022",
abstract = "The main pathological hallmark of diabetes is the loss of functional β-cells. Among several types of β-cell death in diabetes, the
involvement of ferroptosis remains elusive. Therefore, we investigated the potential of diabetes-mimicking factors: high glucose
(HG), proinflammatory cytokines, hydrogen peroxide (H2O2), or diabetogenic agent streptozotocin (STZ) to induce ferroptosis
of β-cells in vitro. Furthermore, we tested the contribution of ferroptosis to injury of pancreatic islets in an STZ-induced
in vivo diabetic model. All in vitro treatments increased loss of Rin-5F cells along with the accumulation of reactive oxygen
species, lipid peroxides and iron, inactivation of NF-E2-related factor 2 (Nrf2), and decrease in glutathione peroxidase 4
expression and mitochondrial membrane potential (MMP). Ferrostatin 1 (Fer-1), ferroptosis inhibitor, diminished the abovestated effects and rescued cells from death in case of HG, STZ, and H2O2 treatments, while failed to increase MMP and to
attenuate cell death after the cytokines’ treatment. Moreover, Fer-1 protected pancreatic islets from STZ-induced injury in
diabetic in vivo model, since it decreased infiltration of macrophages and accumulation of lipid peroxides and increased the
population of insulin-positive cells. Such results revealed differences between diabetogenic stimuli in determining the destiny of
β-cells, emerging HG, H2O2, and STZ, but not cytokines, as contributing factors to ferroptosis and shed new light on an
antidiabetic strategy based on Nrf2 activation. Thus, targeting ferroptosis in diabetes might be a promising new approach for
preservation of the β-cell population. Our results obtained from in vivo study strongly justify this approach.",
publisher = "London:Hindawi",
journal = "Oxidative Medicine and Cellular Longevity",
title = "Ferroptosis as a Novel Determinant of β-Cell Death in Diabetic Conditions",
volume = "2022",
doi = "10.1155/2022/3873420",
pages = "3873420"
}

Stančić, A., Saksida, T., Markelić, M., Vučetić, M., Grigorov, I., Martinović, V., Mićanović, D., Ivanović, A., Veličković, K., Savić, N.,& Otašević, V.. (2022). Ferroptosis as a Novel Determinant of β-Cell Death in Diabetic Conditions. in Oxidative Medicine and Cellular Longevity
London:Hindawi., 2022, 3873420.
https://doi.org/10.1155/2022/3873420

Stančić A, Saksida T, Markelić M, Vučetić M, Grigorov I, Martinović V, Mićanović D, Ivanović A, Veličković K, Savić N, Otašević V. Ferroptosis as a Novel Determinant of β-Cell Death in Diabetic Conditions. in Oxidative Medicine and Cellular Longevity. 2022;2022:3873420.
doi:10.1155/2022/3873420 .

Stančić, Ana, Saksida, Tamara, Markelić, Milica, Vučetić, Milica, Grigorov, Ilijana, Martinović, Vesna, Mićanović, Dragica, Ivanović, Anđelija, Veličković, Ksenija, Savić, Nevena, Otašević, Vesna, "Ferroptosis as a Novel Determinant of β-Cell Death in Diabetic Conditions" in Oxidative Medicine and Cellular Longevity, 2022 (2022):3873420,
https://doi.org/10.1155/2022/3873420 . .

TY  - CONF
AU  - Stančić, Ana
AU  - Saksida, Tamara
AU  - Markelić, Milica
AU  - Vučetić, Milica
AU  - Grigorov, Ilijana
AU  - Martinović, Vesna
AU  - Ivanović, Anđelija
AU  - Veličković, Ksenija
AU  - Otašević, Vesna
PY  - 2021
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/4899
AB  - Diabetes is a complex metabolic disorder which incidence rises in the epidemic fashion, suggesting the urgent need for new therapies. Its main pathological hallmark is loss of functional β-cells, and to date, several types of β-cell death have been described – necrosis, apoptosis, and autophagy. However, the role of ferroptosis in reducing β-cell population in diabetes remains elusive. In this study we aimed to examine whether and how this type of cell death is implicated in regulation of β-cell destiny in diabetes. For that purpose, Rin-5F insulin-producing pancreatic cells were treated with diabetes-mimicking factors – high glucose (HG) and H2O2, as well with commonly used diabetogenic agent streptozotocin (STZ). Results showed that HG, H2O2 and STZ induce the death of Rin-5F cells along with the accumulation of reactive oxygen species, lipid peroxides and iron; inactivation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and decrease in glutathione peroxidase 4 expression. This is consistent with the effect of the treatment with RSL-3, a well-known inducer of ferroptosis. Ferrostatin-1, a ferroptosis inhibitor, diminished above-stated effects and rescued cells from death. Our data revealed that β-cells underwent ferroptotic cell death under diabetogenic conditions. Results also implicate HG and H2O2 as contributing factors to ferroptosis of β-cells and suggest the novel mechanism of STZ diabetogenic action. Furthermore, the results shed a new light on antidiabetic strategy based on Nrf2 activation, putting it into the anti-ferroptotic context. In close, targeting ferroptosis in diabetes might be a new promising therapeutic approach based on preservation of β-cell population.
PB  - Belgrade: Faculty of Chemistry: Serbian Biochemical Society
C3  - Serbian Biochemical Society Tenth Conference: with international participation: Biochemical Insights into Molecular Mechanisms; 2021 Sep 24; Kragujevac, Serbia
T1  - Ferroptosis as a novel determinant of β-cell death in diabetic conditions
SP  - 146
EP  - 147
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_4899
ER  - 

@conference{
author = "Stančić, Ana and Saksida, Tamara and Markelić, Milica and Vučetić, Milica and Grigorov, Ilijana and Martinović, Vesna and Ivanović, Anđelija and Veličković, Ksenija and Otašević, Vesna",
year = "2021",
abstract = "Diabetes is a complex metabolic disorder which incidence rises in the epidemic fashion, suggesting the urgent need for new therapies. Its main pathological hallmark is loss of functional β-cells, and to date, several types of β-cell death have been described – necrosis, apoptosis, and autophagy. However, the role of ferroptosis in reducing β-cell population in diabetes remains elusive. In this study we aimed to examine whether and how this type of cell death is implicated in regulation of β-cell destiny in diabetes. For that purpose, Rin-5F insulin-producing pancreatic cells were treated with diabetes-mimicking factors – high glucose (HG) and H2O2, as well with commonly used diabetogenic agent streptozotocin (STZ). Results showed that HG, H2O2 and STZ induce the death of Rin-5F cells along with the accumulation of reactive oxygen species, lipid peroxides and iron; inactivation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and decrease in glutathione peroxidase 4 expression. This is consistent with the effect of the treatment with RSL-3, a well-known inducer of ferroptosis. Ferrostatin-1, a ferroptosis inhibitor, diminished above-stated effects and rescued cells from death. Our data revealed that β-cells underwent ferroptotic cell death under diabetogenic conditions. Results also implicate HG and H2O2 as contributing factors to ferroptosis of β-cells and suggest the novel mechanism of STZ diabetogenic action. Furthermore, the results shed a new light on antidiabetic strategy based on Nrf2 activation, putting it into the anti-ferroptotic context. In close, targeting ferroptosis in diabetes might be a new promising therapeutic approach based on preservation of β-cell population.",
publisher = "Belgrade: Faculty of Chemistry: Serbian Biochemical Society",
journal = "Serbian Biochemical Society Tenth Conference: with international participation: Biochemical Insights into Molecular Mechanisms; 2021 Sep 24; Kragujevac, Serbia",
title = "Ferroptosis as a novel determinant of β-cell death in diabetic conditions",
pages = "146-147",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_4899"
}

Stančić, A., Saksida, T., Markelić, M., Vučetić, M., Grigorov, I., Martinović, V., Ivanović, A., Veličković, K.,& Otašević, V.. (2021). Ferroptosis as a novel determinant of β-cell death in diabetic conditions. in Serbian Biochemical Society Tenth Conference: with international participation: Biochemical Insights into Molecular Mechanisms; 2021 Sep 24; Kragujevac, Serbia
Belgrade: Faculty of Chemistry: Serbian Biochemical Society., 146-147.
https://hdl.handle.net/21.15107/rcub_ibiss_4899

Stančić A, Saksida T, Markelić M, Vučetić M, Grigorov I, Martinović V, Ivanović A, Veličković K, Otašević V. Ferroptosis as a novel determinant of β-cell death in diabetic conditions. in Serbian Biochemical Society Tenth Conference: with international participation: Biochemical Insights into Molecular Mechanisms; 2021 Sep 24; Kragujevac, Serbia. 2021;:146-147.
https://hdl.handle.net/21.15107/rcub_ibiss_4899 .

Stančić, Ana, Saksida, Tamara, Markelić, Milica, Vučetić, Milica, Grigorov, Ilijana, Martinović, Vesna, Ivanović, Anđelija, Veličković, Ksenija, Otašević, Vesna, "Ferroptosis as a novel determinant of β-cell death in diabetic conditions" in Serbian Biochemical Society Tenth Conference: with international participation: Biochemical Insights into Molecular Mechanisms; 2021 Sep 24; Kragujevac, Serbia (2021):146-147,
https://hdl.handle.net/21.15107/rcub_ibiss_4899 .

TY  - JOUR
AU  - Pajares, Marta
AU  - Jimenez-Moreno, Natalia
AU  - Dias, Irundika H. K.
AU  - Debelec, Bilge
AU  - Vučetić, Milica
AU  - Fladmark, Kari E.
AU  - Basaga, Huveyda
AU  - Ribaric, Sarno
AU  - Milisav, Irina
AU  - Cuadrado, Antonio
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2327
AB  - Intracellular proteolysis is critical to maintain timely degradation of
   altered proteins including oxidized proteins. This review attempts to
   summarize the most relevant findings about oxidant protein modification,
   as well as the impact of reactive oxygen species on the proteolytic
   systems that regulate cell response to an oxidant environment: the
   ubiquitin-proteasome system (UPS), autophagy and the unfolded protein
   response (UPR). In the presence of an oxidant environment, these systems
   are critical to ensure proteostasis and cell survival. An example of
   altered degradation of oxidized proteins in pathology is provided for
   neurodegenerative diseases. Future work will determine if protein
   oxidation is a valid target to combat proteinopathics., (C) 2015 The
   Authors. Published by Elsevier B.V.
T2  - Redox Biology
T1  - Redox control of protein degradation
VL  - 6
DO  - 10.1016/j.redox.2015.07.003
SP  - 409
EP  - 420
ER  - 

@article{
author = "Pajares, Marta and Jimenez-Moreno, Natalia and Dias, Irundika H. K. and Debelec, Bilge and Vučetić, Milica and Fladmark, Kari E. and Basaga, Huveyda and Ribaric, Sarno and Milisav, Irina and Cuadrado, Antonio",
year = "2015",
abstract = "Intracellular proteolysis is critical to maintain timely degradation of
   altered proteins including oxidized proteins. This review attempts to
   summarize the most relevant findings about oxidant protein modification,
   as well as the impact of reactive oxygen species on the proteolytic
   systems that regulate cell response to an oxidant environment: the
   ubiquitin-proteasome system (UPS), autophagy and the unfolded protein
   response (UPR). In the presence of an oxidant environment, these systems
   are critical to ensure proteostasis and cell survival. An example of
   altered degradation of oxidized proteins in pathology is provided for
   neurodegenerative diseases. Future work will determine if protein
   oxidation is a valid target to combat proteinopathics., (C) 2015 The
   Authors. Published by Elsevier B.V.",
journal = "Redox Biology",
title = "Redox control of protein degradation",
volume = "6",
doi = "10.1016/j.redox.2015.07.003",
pages = "409-420"
}

Pajares, M., Jimenez-Moreno, N., Dias, I. H. K., Debelec, B., Vučetić, M., Fladmark, K. E., Basaga, H., Ribaric, S., Milisav, I.,& Cuadrado, A.. (2015). Redox control of protein degradation. in Redox Biology, 6, 409-420.
https://doi.org/10.1016/j.redox.2015.07.003

Pajares M, Jimenez-Moreno N, Dias IHK, Debelec B, Vučetić M, Fladmark KE, Basaga H, Ribaric S, Milisav I, Cuadrado A. Redox control of protein degradation. in Redox Biology. 2015;6:409-420.
doi:10.1016/j.redox.2015.07.003 .

Pajares, Marta, Jimenez-Moreno, Natalia, Dias, Irundika H. K., Debelec, Bilge, Vučetić, Milica, Fladmark, Kari E., Basaga, Huveyda, Ribaric, Sarno, Milisav, Irina, Cuadrado, Antonio, "Redox control of protein degradation" in Redox Biology, 6 (2015):409-420,
https://doi.org/10.1016/j.redox.2015.07.003 . .

TY  - JOUR
AU  - Macanović, Biljana
AU  - Vučetić, Milica
AU  - Janković, Aleksandra
AU  - Stančić, Ana
AU  - Buzadžić, Biljana J.
AU  - Garalejić, Eliana
AU  - Korać, Aleksandra
AU  - Korać, Bato
AU  - Otašević, Vesna
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2090
AB  - Background. Semen analysis is the cornerstone in the evaluation of male
   (in) fertility. However, there are men with normal semen tests but with
   impaired fertilizing ability, as well as fertile men with poor sperm
   characteristics. Thus, there is rising interest to find novel parameters
   that will help to predict and define the functional capacity of
   spermatozoa. Methods. We examined whether there is a correlation between
   semen parameters (count, progressive motility, and morphology) and
   protein expression/activity of antioxidative defense enzymes in seminal
   plasma from 10 normospermic subjects. Results. Sperm progressive
   motility was in positive correlation with seminal plasma protein
   expression of both superoxide dismutase (SOD) isoforms (MnSOD and
   CuZnSOD) and catalase. Also, positive correlation was observed between
   sperm count and MnSOD protein expression, as well as between sperm
   morphology and protein expression of catalase in seminal plasma. In
   contrast, protein expression of glutathione peroxidase was not in
   correlation with any sperm parameter, while its activity negatively
   correlated with sperm morphology and motility. Conclusions. These data
   suggest that evaluation of protein expression of antioxidative defense
   enzymes in seminal plasma might be of importance in the evaluation of
   male fertility status and that could be used as an additional biomarker
   along with classic semen analysis in assessment of semen quality.
T2  - Disease Markers
T1  - Correlation between Sperm Parameters and Protein Expression of
 Antioxidative Defense Enzymes in Seminal Plasma: A Pilot Study
IS  - 436236
DO  - 10.1155/2015/436236
ER  - 

@article{
author = "Macanović, Biljana and Vučetić, Milica and Janković, Aleksandra and Stančić, Ana and Buzadžić, Biljana J. and Garalejić, Eliana and Korać, Aleksandra and Korać, Bato and Otašević, Vesna",
year = "2015",
abstract = "Background. Semen analysis is the cornerstone in the evaluation of male
   (in) fertility. However, there are men with normal semen tests but with
   impaired fertilizing ability, as well as fertile men with poor sperm
   characteristics. Thus, there is rising interest to find novel parameters
   that will help to predict and define the functional capacity of
   spermatozoa. Methods. We examined whether there is a correlation between
   semen parameters (count, progressive motility, and morphology) and
   protein expression/activity of antioxidative defense enzymes in seminal
   plasma from 10 normospermic subjects. Results. Sperm progressive
   motility was in positive correlation with seminal plasma protein
   expression of both superoxide dismutase (SOD) isoforms (MnSOD and
   CuZnSOD) and catalase. Also, positive correlation was observed between
   sperm count and MnSOD protein expression, as well as between sperm
   morphology and protein expression of catalase in seminal plasma. In
   contrast, protein expression of glutathione peroxidase was not in
   correlation with any sperm parameter, while its activity negatively
   correlated with sperm morphology and motility. Conclusions. These data
   suggest that evaluation of protein expression of antioxidative defense
   enzymes in seminal plasma might be of importance in the evaluation of
   male fertility status and that could be used as an additional biomarker
   along with classic semen analysis in assessment of semen quality.",
journal = "Disease Markers",
title = "Correlation between Sperm Parameters and Protein Expression of
 Antioxidative Defense Enzymes in Seminal Plasma: A Pilot Study",
number = "436236",
doi = "10.1155/2015/436236"
}

Macanović, B., Vučetić, M., Janković, A., Stančić, A., Buzadžić, B. J., Garalejić, E., Korać, A., Korać, B.,& Otašević, V.. (2015). Correlation between Sperm Parameters and Protein Expression of
 Antioxidative Defense Enzymes in Seminal Plasma: A Pilot Study. in Disease Markers(436236).
https://doi.org/10.1155/2015/436236

Macanović B, Vučetić M, Janković A, Stančić A, Buzadžić BJ, Garalejić E, Korać A, Korać B, Otašević V. Correlation between Sperm Parameters and Protein Expression of
 Antioxidative Defense Enzymes in Seminal Plasma: A Pilot Study. in Disease Markers. 2015;(436236).
doi:10.1155/2015/436236 .

Macanović, Biljana, Vučetić, Milica, Janković, Aleksandra, Stančić, Ana, Buzadžić, Biljana J., Garalejić, Eliana, Korać, Aleksandra, Korać, Bato, Otašević, Vesna, "Correlation between Sperm Parameters and Protein Expression of
 Antioxidative Defense Enzymes in Seminal Plasma: A Pilot Study" in Disease Markers, no. 436236 (2015),
https://doi.org/10.1155/2015/436236 . .

TY  - JOUR
AU  - Veličković, Ksenija
AU  - Čvoro, Aleksandra
AU  - Srdić, Biljana
AU  - Stokić, Edita
AU  - Markelić, Milica
AU  - Golić, Igor
AU  - Otašević, Vesna
AU  - Stančić, Ana
AU  - Janković, Aleksandra
AU  - Vučetić, Milica
AU  - Buzadžić, Biljana J.
AU  - Korać, Bato
AU  - Korać, Aleksandra
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2294
AB  - Context: Brown adipose tissue (BAT) has the unique ability of generating
   heat due to the expression of mitochondrial uncoupling protein 1 (UCP1).
   A recent discovery regarding functional BAT in adult humans has
   increased interest in the molecular pathways of BAT development and
   functionality. An important role for estrogen in white adipose tissue
   was shown, but the possible role of estrogen in human fetal BAT (fBAT)
   is unclear.
   Objective: The objective of this study was to determine whether human
   fBAT expresses estrogen receptor alpha (ER alpha) and ER beta. In
   addition, we examined their localization as well as their correlation
   with crucial proteins involved in BAT differentiation, proliferation,
   mitochondriogenesis and thermogenesis including peroxisome
   proliferator-activated receptor gamma (PPAR gamma), proliferating cell
   nuclear antigen (PCNA), PPAR gamma-coactivator-1 alpha (PGC-1 alpha),
   and UCP1.
   Design: The fBAT was obtained from 4 human male fetuses aged 15, 17, 20,
   and 23 weeks gestation. ER alpha and ER beta expression was assessed
   using Western blotting, immunohistochemistry, and immunocytochemistry.
   Possible correlations with PPAR gamma, PCNA, PGC-1 alpha, and UCP1 were
   examined by double immunofluorescence.
   Results: Both ER alpha and ER beta were expressed in human fBAT, with ER
   alpha being dominant. Unlike ER beta, which was present only in mature
   brown adipocytes, we detected ER alpha in mature adipocytes,
   preadipocytes, mesenchymal and endothelial cells. In addition, double
   immunofluorescence supported the notion that differentiation in fBAT
   probably involves ER alpha. Immunocytochemical analysis revealed
   mitochondrial localization of both receptors.
   Conclusion: The expression of both ER alpha and ER beta in human fBAT
   suggests a role for estrogen in its development, primarily via ER alpha.
   In addition, our results indicate that fBAT mitochondria could be
   targeted by estrogens and pointed out the possible role of both ERs in
   mitochondriogenesis.
T2  - Journal of Clinical Endocrinology & Metabolism
T1  - Expression and Subcellular Localization of Estrogen Receptors alpha and
 beta in Human Fetal Brown Adipose Tissue
IS  - 1
VL  - 99
DO  - 10.1210/jc.2013-2017
SP  - 151
EP  - 159
ER  - 

@article{
author = "Veličković, Ksenija and Čvoro, Aleksandra and Srdić, Biljana and Stokić, Edita and Markelić, Milica and Golić, Igor and Otašević, Vesna and Stančić, Ana and Janković, Aleksandra and Vučetić, Milica and Buzadžić, Biljana J. and Korać, Bato and Korać, Aleksandra",
year = "2014",
abstract = "Context: Brown adipose tissue (BAT) has the unique ability of generating
   heat due to the expression of mitochondrial uncoupling protein 1 (UCP1).
   A recent discovery regarding functional BAT in adult humans has
   increased interest in the molecular pathways of BAT development and
   functionality. An important role for estrogen in white adipose tissue
   was shown, but the possible role of estrogen in human fetal BAT (fBAT)
   is unclear.
   Objective: The objective of this study was to determine whether human
   fBAT expresses estrogen receptor alpha (ER alpha) and ER beta. In
   addition, we examined their localization as well as their correlation
   with crucial proteins involved in BAT differentiation, proliferation,
   mitochondriogenesis and thermogenesis including peroxisome
   proliferator-activated receptor gamma (PPAR gamma), proliferating cell
   nuclear antigen (PCNA), PPAR gamma-coactivator-1 alpha (PGC-1 alpha),
   and UCP1.
   Design: The fBAT was obtained from 4 human male fetuses aged 15, 17, 20,
   and 23 weeks gestation. ER alpha and ER beta expression was assessed
   using Western blotting, immunohistochemistry, and immunocytochemistry.
   Possible correlations with PPAR gamma, PCNA, PGC-1 alpha, and UCP1 were
   examined by double immunofluorescence.
   Results: Both ER alpha and ER beta were expressed in human fBAT, with ER
   alpha being dominant. Unlike ER beta, which was present only in mature
   brown adipocytes, we detected ER alpha in mature adipocytes,
   preadipocytes, mesenchymal and endothelial cells. In addition, double
   immunofluorescence supported the notion that differentiation in fBAT
   probably involves ER alpha. Immunocytochemical analysis revealed
   mitochondrial localization of both receptors.
   Conclusion: The expression of both ER alpha and ER beta in human fBAT
   suggests a role for estrogen in its development, primarily via ER alpha.
   In addition, our results indicate that fBAT mitochondria could be
   targeted by estrogens and pointed out the possible role of both ERs in
   mitochondriogenesis.",
journal = "Journal of Clinical Endocrinology & Metabolism",
title = "Expression and Subcellular Localization of Estrogen Receptors alpha and
 beta in Human Fetal Brown Adipose Tissue",
number = "1",
volume = "99",
doi = "10.1210/jc.2013-2017",
pages = "151-159"
}

Veličković, K., Čvoro, A., Srdić, B., Stokić, E., Markelić, M., Golić, I., Otašević, V., Stančić, A., Janković, A., Vučetić, M., Buzadžić, B. J., Korać, B.,& Korać, A.. (2014). Expression and Subcellular Localization of Estrogen Receptors alpha and
 beta in Human Fetal Brown Adipose Tissue. in Journal of Clinical Endocrinology & Metabolism, 99(1), 151-159.
https://doi.org/10.1210/jc.2013-2017

Veličković K, Čvoro A, Srdić B, Stokić E, Markelić M, Golić I, Otašević V, Stančić A, Janković A, Vučetić M, Buzadžić BJ, Korać B, Korać A. Expression and Subcellular Localization of Estrogen Receptors alpha and
 beta in Human Fetal Brown Adipose Tissue. in Journal of Clinical Endocrinology & Metabolism. 2014;99(1):151-159.
doi:10.1210/jc.2013-2017 .

Veličković, Ksenija, Čvoro, Aleksandra, Srdić, Biljana, Stokić, Edita, Markelić, Milica, Golić, Igor, Otašević, Vesna, Stančić, Ana, Janković, Aleksandra, Vučetić, Milica, Buzadžić, Biljana J., Korać, Bato, Korać, Aleksandra, "Expression and Subcellular Localization of Estrogen Receptors alpha and
 beta in Human Fetal Brown Adipose Tissue" in Journal of Clinical Endocrinology & Metabolism, 99, no. 1 (2014):151-159,
https://doi.org/10.1210/jc.2013-2017 . .

TY  - JOUR
AU  - Velickovic, Ksenija
AU  - Markelic, Milica
AU  - Golic, Igor
AU  - Otašević, Vesna
AU  - Stančić, Ana
AU  - Janković, Aleksandra
AU  - Vucetic, Milica
AU  - Buzadžić, Biljana J.
AU  - Korać, Bato
AU  - Korac, Aleksandra
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2227
AB  - Nitric oxide (NO) and vasoactive intestinal polypeptide (VIP) are
   important intestinal neurotransmitters that coexist in the gut enteric
   nervous system and play an important role in intestinal physiology
   (e.g., absorption, motility, fluid secretion and smooth muscle
   relaxation). It is also known that cold exposure alters several aspects
   of gastrointestinal physiology and induces hyperphagia to meet increased
   metabolic demands, but there are no data regarding NO and VIP
   involvement in intestinal response during acclimation to cold. The
   objective of this study was to determine the influence of long-term
   l-arginine supplementation on the expression of the three isoforms of
   nitric oxide synthase (NOS) and VIP in small intestine of rats
   acclimated to room temperature or cold.
   Animals (six per group) acclimated to room temperature (22 +/- A 1 A
   degrees C) and cold (4 +/- A 1 A degrees C), respectively, were treated
   with 2.25 \% l-arginine, a substrate for NOSs, or with 0.01 \% N
   (omega)-nitro-l-arginine methyl ester, an inhibitor of NOSs, for 45
   days. The topographical distribution of VIP and NOSs expression in small
   intestine was studied by immunohistochemistry, and ImageJ software was
   used for semiquantitative densitometric analysis of their
   immunoexpression.
   Long-term dietary l-arginine supplementation increases VIP and NOSs
   immunoexpression at room temperature while at cold increases the
   endothelial NOS, inducible NOS and VIP but decrease neuronal NOS in rat
   small intestine.
   Our results demonstrate that long-term dietary l-arginine
   supplementation modulates NOSs and VIP immunoexpression in rat small
   intestine with respect to ambient temperature, pointing out the eNOS as
   a predominant NOS isoform with an immunoexpression pattern similar to
   VIP.
T2  - European Journal of Nutrition
T1  - Long-term dietary L-arginine supplementation increases endothelial
 nitric oxide synthase and vasoactive intestinal peptide immunoexpression
 in rat small intestine
IS  - 3
VL  - 53
DO  - 10.1007/s00394-013-0585-8
SP  - 813
EP  - 821
ER  - 

@article{
author = "Velickovic, Ksenija and Markelic, Milica and Golic, Igor and Otašević, Vesna and Stančić, Ana and Janković, Aleksandra and Vucetic, Milica and Buzadžić, Biljana J. and Korać, Bato and Korac, Aleksandra",
year = "2014",
abstract = "Nitric oxide (NO) and vasoactive intestinal polypeptide (VIP) are
   important intestinal neurotransmitters that coexist in the gut enteric
   nervous system and play an important role in intestinal physiology
   (e.g., absorption, motility, fluid secretion and smooth muscle
   relaxation). It is also known that cold exposure alters several aspects
   of gastrointestinal physiology and induces hyperphagia to meet increased
   metabolic demands, but there are no data regarding NO and VIP
   involvement in intestinal response during acclimation to cold. The
   objective of this study was to determine the influence of long-term
   l-arginine supplementation on the expression of the three isoforms of
   nitric oxide synthase (NOS) and VIP in small intestine of rats
   acclimated to room temperature or cold.
   Animals (six per group) acclimated to room temperature (22 +/- A 1 A
   degrees C) and cold (4 +/- A 1 A degrees C), respectively, were treated
   with 2.25 \% l-arginine, a substrate for NOSs, or with 0.01 \% N
   (omega)-nitro-l-arginine methyl ester, an inhibitor of NOSs, for 45
   days. The topographical distribution of VIP and NOSs expression in small
   intestine was studied by immunohistochemistry, and ImageJ software was
   used for semiquantitative densitometric analysis of their
   immunoexpression.
   Long-term dietary l-arginine supplementation increases VIP and NOSs
   immunoexpression at room temperature while at cold increases the
   endothelial NOS, inducible NOS and VIP but decrease neuronal NOS in rat
   small intestine.
   Our results demonstrate that long-term dietary l-arginine
   supplementation modulates NOSs and VIP immunoexpression in rat small
   intestine with respect to ambient temperature, pointing out the eNOS as
   a predominant NOS isoform with an immunoexpression pattern similar to
   VIP.",
journal = "European Journal of Nutrition",
title = "Long-term dietary L-arginine supplementation increases endothelial
 nitric oxide synthase and vasoactive intestinal peptide immunoexpression
 in rat small intestine",
number = "3",
volume = "53",
doi = "10.1007/s00394-013-0585-8",
pages = "813-821"
}

Velickovic, K., Markelic, M., Golic, I., Otašević, V., Stančić, A., Janković, A., Vucetic, M., Buzadžić, B. J., Korać, B.,& Korac, A.. (2014). Long-term dietary L-arginine supplementation increases endothelial
 nitric oxide synthase and vasoactive intestinal peptide immunoexpression
 in rat small intestine. in European Journal of Nutrition, 53(3), 813-821.
https://doi.org/10.1007/s00394-013-0585-8

Velickovic K, Markelic M, Golic I, Otašević V, Stančić A, Janković A, Vucetic M, Buzadžić BJ, Korać B, Korac A. Long-term dietary L-arginine supplementation increases endothelial
 nitric oxide synthase and vasoactive intestinal peptide immunoexpression
 in rat small intestine. in European Journal of Nutrition. 2014;53(3):813-821.
doi:10.1007/s00394-013-0585-8 .

Velickovic, Ksenija, Markelic, Milica, Golic, Igor, Otašević, Vesna, Stančić, Ana, Janković, Aleksandra, Vucetic, Milica, Buzadžić, Biljana J., Korać, Bato, Korac, Aleksandra, "Long-term dietary L-arginine supplementation increases endothelial
 nitric oxide synthase and vasoactive intestinal peptide immunoexpression
 in rat small intestine" in European Journal of Nutrition, 53, no. 3 (2014):813-821,
https://doi.org/10.1007/s00394-013-0585-8 . .

TY  - JOUR
AU  - Janković, Aleksandra
AU  - Korac, Aleksandra
AU  - Srdic-Galic, Biljana
AU  - Buzadžić, Biljana J.
AU  - Otašević, Vesna
AU  - Stančić, Ana
AU  - Vucetic, Milica
AU  - Markelic, Milica
AU  - Velickovic, Ksenija
AU  - Golic, Igor
AU  - Korać, Bato
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2220
AB  - Objective. Metabolic homeostasis depends on adipocyte metabolic
   responses/processes, most of which are redox-regulated. Besides,
   visceral and subcutaneous adipose tissues (VAT and SAT, respectively)
   differ metabolically and in their contribution to metabolic
   complications, but their redox characteristics in humans are still
   unknown. To understand the molecular mechanisms of metabolic syndrome
   development, we analysed the redox characteristics of VAT and SAT in
   groups with various body weights and metabolic risks.
   Material and Methods. Fifty premenopausal women were classified
   according to body mass index into normal-weight and obese groups, and
   these groups were further sub-classified into metabolically healthy and
   metabolically obese ({''}at risk{''}) based on the homeostasis model
   assessment of insulin resistance (HOMA-IR) index and the triglyceride,
   total-, LDL- and HDL-cholesterol levels. Antioxidant components, NADPH
   oxidase protein and 4-hydroxynonenal (4-HNE) levels were analysed in VAT
   and SAT.
   Results. Compared with the SAT, the VAT showed a higher basal level of
   glutathione (GSH) and GSH-dependent enzyme activities. Compared with the
   metabolically healthy normal-weight controls, the obese groups of women
   showed lower GSH levels in both depots. However, in these groups,
   additional prooxidative changes (increased NADPH oxidase and 4-HNE and
   decreased levels of SOD and/or CAT) were observed only in VAT.
   Conclusions. Because of the critical role of thiol-redox homeostasis in
   lipogenesis, interdepot-differences in the GSH-dependent antioxidant
   part may be connected to the higher metabolic activity found in VAT.
   Analogously, the lower GSH levels that occur during obesity and the
   corresponding additional redox imbalance may be signs of VAT metabolic
   dysfunction that underlie the subsequent metabolic impairment. (C) 2014
   Elsevier Inc. All rights reserved.
T2  - Metabolism-Clinical and Experimental
T1  - Differences in the redox status of human visceral and subcutaneous
 adipose tissues - relationships to obesity and metabolic risk
IS  - 5
VL  - 63
DO  - 10.1016/j.metabol.2014.01.009
SP  - 661
EP  - 671
ER  - 

@article{
author = "Janković, Aleksandra and Korac, Aleksandra and Srdic-Galic, Biljana and Buzadžić, Biljana J. and Otašević, Vesna and Stančić, Ana and Vucetic, Milica and Markelic, Milica and Velickovic, Ksenija and Golic, Igor and Korać, Bato",
year = "2014",
abstract = "Objective. Metabolic homeostasis depends on adipocyte metabolic
   responses/processes, most of which are redox-regulated. Besides,
   visceral and subcutaneous adipose tissues (VAT and SAT, respectively)
   differ metabolically and in their contribution to metabolic
   complications, but their redox characteristics in humans are still
   unknown. To understand the molecular mechanisms of metabolic syndrome
   development, we analysed the redox characteristics of VAT and SAT in
   groups with various body weights and metabolic risks.
   Material and Methods. Fifty premenopausal women were classified
   according to body mass index into normal-weight and obese groups, and
   these groups were further sub-classified into metabolically healthy and
   metabolically obese ({''}at risk{''}) based on the homeostasis model
   assessment of insulin resistance (HOMA-IR) index and the triglyceride,
   total-, LDL- and HDL-cholesterol levels. Antioxidant components, NADPH
   oxidase protein and 4-hydroxynonenal (4-HNE) levels were analysed in VAT
   and SAT.
   Results. Compared with the SAT, the VAT showed a higher basal level of
   glutathione (GSH) and GSH-dependent enzyme activities. Compared with the
   metabolically healthy normal-weight controls, the obese groups of women
   showed lower GSH levels in both depots. However, in these groups,
   additional prooxidative changes (increased NADPH oxidase and 4-HNE and
   decreased levels of SOD and/or CAT) were observed only in VAT.
   Conclusions. Because of the critical role of thiol-redox homeostasis in
   lipogenesis, interdepot-differences in the GSH-dependent antioxidant
   part may be connected to the higher metabolic activity found in VAT.
   Analogously, the lower GSH levels that occur during obesity and the
   corresponding additional redox imbalance may be signs of VAT metabolic
   dysfunction that underlie the subsequent metabolic impairment. (C) 2014
   Elsevier Inc. All rights reserved.",
journal = "Metabolism-Clinical and Experimental",
title = "Differences in the redox status of human visceral and subcutaneous
 adipose tissues - relationships to obesity and metabolic risk",
number = "5",
volume = "63",
doi = "10.1016/j.metabol.2014.01.009",
pages = "661-671"
}

Janković, A., Korac, A., Srdic-Galic, B., Buzadžić, B. J., Otašević, V., Stančić, A., Vucetic, M., Markelic, M., Velickovic, K., Golic, I.,& Korać, B.. (2014). Differences in the redox status of human visceral and subcutaneous
 adipose tissues - relationships to obesity and metabolic risk. in Metabolism-Clinical and Experimental, 63(5), 661-671.
https://doi.org/10.1016/j.metabol.2014.01.009

Janković A, Korac A, Srdic-Galic B, Buzadžić BJ, Otašević V, Stančić A, Vucetic M, Markelic M, Velickovic K, Golic I, Korać B. Differences in the redox status of human visceral and subcutaneous
 adipose tissues - relationships to obesity and metabolic risk. in Metabolism-Clinical and Experimental. 2014;63(5):661-671.
doi:10.1016/j.metabol.2014.01.009 .

Janković, Aleksandra, Korac, Aleksandra, Srdic-Galic, Biljana, Buzadžić, Biljana J., Otašević, Vesna, Stančić, Ana, Vucetic, Milica, Markelic, Milica, Velickovic, Ksenija, Golic, Igor, Korać, Bato, "Differences in the redox status of human visceral and subcutaneous
 adipose tissues - relationships to obesity and metabolic risk" in Metabolism-Clinical and Experimental, 63, no. 5 (2014):661-671,
https://doi.org/10.1016/j.metabol.2014.01.009 . .