TY  - JOUR
AU  - Stepanović, Ana
AU  - Terzić Jovanović, Nataša
AU  - Korać, Aleksandra
AU  - Zlatović, Mario
AU  - Nikolić, Igor
AU  - Opsenica, Igor
AU  - Pešić, Milica
PY  - 2024
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6664
AB  - Two novel hybrid compounds, CON1 and CON2, have been developed by combining sclareol (SC) and doxorubicin (DOX) into a single molecular entity. These hybrid compounds have a 1:1 molar ratio of covalently linked SC and DOX. They have demonstrated promising anticancer properties, especially in glioblastoma cells, and have also shown potential in treating multidrug-resistant (MDR) cancer cells that express the P-glycoprotein (P-gp) membrane transporter. CON1 and CON2 form nanoparticles, as confirmed by Zetasizer, transmission electron microscopy (TEM), and chemical modeling. TEM also showed that CON1 and CON2 can be found in glioblastoma cells, specifically in the cytoplasm, different organelles, nucleus, and nucleolus. To examine the anticancer properties, the U87 glioblastoma cell line, and its corresponding multidrug-resistant U87-TxR cell line, as well as patient-derived astrocytoma grade 3 cells (ASC), were used, while normal human lung fibroblasts were used to determine the selectivity. CON1 and CON2 exhibited better resistance and selectivity profiles than DOX, showing less cytotoxicity, as evidenced by real-time cell analysis, DNA damage determination, cell death induction, mitochondrial respiration, and mitochondrial membrane depolarization studies. Cell cycle analysis and the β-galactosidase activity assay suggested that glioblastoma cells die by senescence following CON1 treatment. Overall, CON1 and CON2 showed great potential as they have better anticancer features than DOX. They are promising candidates for additional preclinical and clinical studies on glioblastoma.
PB  - Elsevier Masson SAS
T2  - Biomedicine & Pharmacotherapy
T1  - Novel hybrid compounds of sclareol and doxorubicin as potential anticancer nanotherapy for glioblastoma
VL  - 174
DO  - 10.1016/j.biopha.2024.116496
SP  - 116496
ER  - 

@article{
author = "Stepanović, Ana and Terzić Jovanović, Nataša and Korać, Aleksandra and Zlatović, Mario and Nikolić, Igor and Opsenica, Igor and Pešić, Milica",
year = "2024",
abstract = "Two novel hybrid compounds, CON1 and CON2, have been developed by combining sclareol (SC) and doxorubicin (DOX) into a single molecular entity. These hybrid compounds have a 1:1 molar ratio of covalently linked SC and DOX. They have demonstrated promising anticancer properties, especially in glioblastoma cells, and have also shown potential in treating multidrug-resistant (MDR) cancer cells that express the P-glycoprotein (P-gp) membrane transporter. CON1 and CON2 form nanoparticles, as confirmed by Zetasizer, transmission electron microscopy (TEM), and chemical modeling. TEM also showed that CON1 and CON2 can be found in glioblastoma cells, specifically in the cytoplasm, different organelles, nucleus, and nucleolus. To examine the anticancer properties, the U87 glioblastoma cell line, and its corresponding multidrug-resistant U87-TxR cell line, as well as patient-derived astrocytoma grade 3 cells (ASC), were used, while normal human lung fibroblasts were used to determine the selectivity. CON1 and CON2 exhibited better resistance and selectivity profiles than DOX, showing less cytotoxicity, as evidenced by real-time cell analysis, DNA damage determination, cell death induction, mitochondrial respiration, and mitochondrial membrane depolarization studies. Cell cycle analysis and the β-galactosidase activity assay suggested that glioblastoma cells die by senescence following CON1 treatment. Overall, CON1 and CON2 showed great potential as they have better anticancer features than DOX. They are promising candidates for additional preclinical and clinical studies on glioblastoma.",
publisher = "Elsevier Masson SAS",
journal = "Biomedicine & Pharmacotherapy",
title = "Novel hybrid compounds of sclareol and doxorubicin as potential anticancer nanotherapy for glioblastoma",
volume = "174",
doi = "10.1016/j.biopha.2024.116496",
pages = "116496"
}

Stepanović, A., Terzić Jovanović, N., Korać, A., Zlatović, M., Nikolić, I., Opsenica, I.,& Pešić, M.. (2024). Novel hybrid compounds of sclareol and doxorubicin as potential anticancer nanotherapy for glioblastoma. in Biomedicine & Pharmacotherapy
Elsevier Masson SAS., 174, 116496.
https://doi.org/10.1016/j.biopha.2024.116496

Stepanović A, Terzić Jovanović N, Korać A, Zlatović M, Nikolić I, Opsenica I, Pešić M. Novel hybrid compounds of sclareol and doxorubicin as potential anticancer nanotherapy for glioblastoma. in Biomedicine & Pharmacotherapy. 2024;174:116496.
doi:10.1016/j.biopha.2024.116496 .

Stepanović, Ana, Terzić Jovanović, Nataša, Korać, Aleksandra, Zlatović, Mario, Nikolić, Igor, Opsenica, Igor, Pešić, Milica, "Novel hybrid compounds of sclareol and doxorubicin as potential anticancer nanotherapy for glioblastoma" in Biomedicine & Pharmacotherapy, 174 (2024):116496,
https://doi.org/10.1016/j.biopha.2024.116496 . .

TY  - CONF
AU  - Zakić, Tamara
AU  - Budnar-Šoškić, Marta
AU  - Stojanović, Sara
AU  - Janković, Aleksandra
AU  - Korać, Aleksandra
AU  - Peković-Vaughan, Vanja
AU  - Korać, Bato
PY  - 2023
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6527
AB  - The precise regulatory mechanisms of interscapular brown adipose tissue (IBAT) thermogenesis are not fully elucidated, especially those in relation to Nuclear factor erythroid 2–related factor 2 (Nrf2). We have recently shown that mice lacking functional Nrf2 (Nrf2KO) at room temperature (RT) depict thermogenic IBAT activity at the structural level. However, gene and protein expression of the main IBAT thermogenic marker uncoupling protein 1 (UCP1), and other redox-metabolic functional parameters, did not align with this apparent thermogenic activation. Here, we investigated the functional activation of IBAT in wild-type (WT) and Nrf2KO mice maintained at RT (24±1°C) or after cold acclimation (45 days, 4±1°C). We performed immunogold labelling of Nrf2 and its closely related transcription factors Nrf1, Nrf3, and nuclear respiratory factor 1 (NRF1) to determine their spatial expression patterns. Next, we measured succinate-based mitochondrial respiration as an indicator of IBAT mitochondrial oxidative function and uncoupling capacity. Electron microscopy confirmed that Nrf2KO mice at RT had the same ultrastructural characteristics as cold-exposed mice, indicating IBAT thermogenic activity. This was associated with increased mitochondrial immunogold reaction of the above redox-sensitive transcription factors indicating their activation in Nrf2KO mice at RT. In contrast to such activated phenotype, respirometry results showed that Nrf2KO mice at RT had no uncoupling activity compared to cold-exposed WT mice. Furthermore, similar respiratory pattern was observed in Nrf2KO mice acclimated to cold, regardless of increased UCP1 expression. These results demonstrate that despite the (ultra)structural recruitment of IBAT in Nrf2KO mice at RT and after cold acclimation, Nrf2 is essential for the full functional thermogenic activation of IBAT and the lack of functional Nrf2 could not be compensated with Nrf1, Nrf3, and NRF1.
PB  - Elsevier
C3  - Redox Biology Congress 2023; 2023 Jun 6-9; Vienna, Austria
T1  - The discrepancy between morphological and functional activation of brown adipose tissue in the absence of functional Nrf2
DO  - 10.1016/j.freeradbiomed.2023.03.109
SP  - 25
ER  - 

@conference{
author = "Zakić, Tamara and Budnar-Šoškić, Marta and Stojanović, Sara and Janković, Aleksandra and Korać, Aleksandra and Peković-Vaughan, Vanja and Korać, Bato",
year = "2023",
abstract = "The precise regulatory mechanisms of interscapular brown adipose tissue (IBAT) thermogenesis are not fully elucidated, especially those in relation to Nuclear factor erythroid 2–related factor 2 (Nrf2). We have recently shown that mice lacking functional Nrf2 (Nrf2KO) at room temperature (RT) depict thermogenic IBAT activity at the structural level. However, gene and protein expression of the main IBAT thermogenic marker uncoupling protein 1 (UCP1), and other redox-metabolic functional parameters, did not align with this apparent thermogenic activation. Here, we investigated the functional activation of IBAT in wild-type (WT) and Nrf2KO mice maintained at RT (24±1°C) or after cold acclimation (45 days, 4±1°C). We performed immunogold labelling of Nrf2 and its closely related transcription factors Nrf1, Nrf3, and nuclear respiratory factor 1 (NRF1) to determine their spatial expression patterns. Next, we measured succinate-based mitochondrial respiration as an indicator of IBAT mitochondrial oxidative function and uncoupling capacity. Electron microscopy confirmed that Nrf2KO mice at RT had the same ultrastructural characteristics as cold-exposed mice, indicating IBAT thermogenic activity. This was associated with increased mitochondrial immunogold reaction of the above redox-sensitive transcription factors indicating their activation in Nrf2KO mice at RT. In contrast to such activated phenotype, respirometry results showed that Nrf2KO mice at RT had no uncoupling activity compared to cold-exposed WT mice. Furthermore, similar respiratory pattern was observed in Nrf2KO mice acclimated to cold, regardless of increased UCP1 expression. These results demonstrate that despite the (ultra)structural recruitment of IBAT in Nrf2KO mice at RT and after cold acclimation, Nrf2 is essential for the full functional thermogenic activation of IBAT and the lack of functional Nrf2 could not be compensated with Nrf1, Nrf3, and NRF1.",
publisher = "Elsevier",
journal = "Redox Biology Congress 2023; 2023 Jun 6-9; Vienna, Austria",
title = "The discrepancy between morphological and functional activation of brown adipose tissue in the absence of functional Nrf2",
doi = "10.1016/j.freeradbiomed.2023.03.109",
pages = "25"
}

Zakić, T., Budnar-Šoškić, M., Stojanović, S., Janković, A., Korać, A., Peković-Vaughan, V.,& Korać, B.. (2023). The discrepancy between morphological and functional activation of brown adipose tissue in the absence of functional Nrf2. in Redox Biology Congress 2023; 2023 Jun 6-9; Vienna, Austria
Elsevier., 25.
https://doi.org/10.1016/j.freeradbiomed.2023.03.109

Zakić T, Budnar-Šoškić M, Stojanović S, Janković A, Korać A, Peković-Vaughan V, Korać B. The discrepancy between morphological and functional activation of brown adipose tissue in the absence of functional Nrf2. in Redox Biology Congress 2023; 2023 Jun 6-9; Vienna, Austria. 2023;:25.
doi:10.1016/j.freeradbiomed.2023.03.109 .

Zakić, Tamara, Budnar-Šoškić, Marta, Stojanović, Sara, Janković, Aleksandra, Korać, Aleksandra, Peković-Vaughan, Vanja, Korać, Bato, "The discrepancy between morphological and functional activation of brown adipose tissue in the absence of functional Nrf2" in Redox Biology Congress 2023; 2023 Jun 6-9; Vienna, Austria (2023):25,
https://doi.org/10.1016/j.freeradbiomed.2023.03.109 . .

TY  - CONF
AU  - Budnar Šoškić, Marta
AU  - Zakić, Tamara
AU  - Korać, Aleksandra
AU  - Korać, Bato
AU  - Janković, Aleksandra
PY  - 2023
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6526
AB  - Тight control of the lipid-deposition function of white adipose tissue (WAT) defines the overall metabolic homeostasis and entails coordinated antioxidant response. We aimed to reveal temporal changes in the antioxidant defence (AD) that is a prerequisite for lipid metabolism in the visceral WAT over 45 days of re-acclimation to room temperature (RT, 22±1 °C) in rats pre-acclimated to cold (45 days, 4±1 °C). The Nuclear factor erythroid 2–related factor 2 (Nrf2) and its downstream antioxidant targets, as well as key lipogenic enzymes were examined in epididymal WAT (eWAT) and compared to the RT-maintained control. Upregulation of Nrf2 protein expression observed from the 1-12th day of re-acclimation was followed by an increase in the glutathione level (3-7th day) and the protein expression of copper, zinc superoxide dismutase (3-12th day), manganese superoxide dismutase (1-12th day), thioredoxin (1-45th day), and glutathione peroxidase (1-45th day). Such time-dependent changes in AD during re-acclimation coincided with increases in the lipogenic enzymes acetyl-CoA carboxylase and fatty acid synthase that were further supported by elevated glyceraldehyde 3-phosphate dehydrogenase and glucose 6-phosphate dehydrogenase protein levels. Observed redox-metabolic integration in eWAT resulted in the restitution of relative eWAT mass on the 12th day of re-acclimation. It can be concluded that Nrf2-coordinated redox-metabolic changes drive the restitution of eWAT lipid depot during the re-acclimation of rats after cold. These results show a novel role of Nrf2 in regulating redox-metabolic signaling under homeostatic conditions and its relevance in visceral adiposity in different metabolic diseases.
PB  - Elsevier
C3  - Redox Biology Congress 2023; 2023 Jun 6-9; Vienna, Austria
T1  - Nrf2 coordinates redox-metabolic homeostasis required for lipid deposition in rat visceral adipose tissue during the re-acclimation of rats after cold
DO  - 10.1016/j.freeradbiomed.2023.03.183
SP  - 26
ER  - 

@conference{
author = "Budnar Šoškić, Marta and Zakić, Tamara and Korać, Aleksandra and Korać, Bato and Janković, Aleksandra",
year = "2023",
abstract = "Тight control of the lipid-deposition function of white adipose tissue (WAT) defines the overall metabolic homeostasis and entails coordinated antioxidant response. We aimed to reveal temporal changes in the antioxidant defence (AD) that is a prerequisite for lipid metabolism in the visceral WAT over 45 days of re-acclimation to room temperature (RT, 22±1 °C) in rats pre-acclimated to cold (45 days, 4±1 °C). The Nuclear factor erythroid 2–related factor 2 (Nrf2) and its downstream antioxidant targets, as well as key lipogenic enzymes were examined in epididymal WAT (eWAT) and compared to the RT-maintained control. Upregulation of Nrf2 protein expression observed from the 1-12th day of re-acclimation was followed by an increase in the glutathione level (3-7th day) and the protein expression of copper, zinc superoxide dismutase (3-12th day), manganese superoxide dismutase (1-12th day), thioredoxin (1-45th day), and glutathione peroxidase (1-45th day). Such time-dependent changes in AD during re-acclimation coincided with increases in the lipogenic enzymes acetyl-CoA carboxylase and fatty acid synthase that were further supported by elevated glyceraldehyde 3-phosphate dehydrogenase and glucose 6-phosphate dehydrogenase protein levels. Observed redox-metabolic integration in eWAT resulted in the restitution of relative eWAT mass on the 12th day of re-acclimation. It can be concluded that Nrf2-coordinated redox-metabolic changes drive the restitution of eWAT lipid depot during the re-acclimation of rats after cold. These results show a novel role of Nrf2 in regulating redox-metabolic signaling under homeostatic conditions and its relevance in visceral adiposity in different metabolic diseases.",
publisher = "Elsevier",
journal = "Redox Biology Congress 2023; 2023 Jun 6-9; Vienna, Austria",
title = "Nrf2 coordinates redox-metabolic homeostasis required for lipid deposition in rat visceral adipose tissue during the re-acclimation of rats after cold",
doi = "10.1016/j.freeradbiomed.2023.03.183",
pages = "26"
}

Budnar Šoškić, M., Zakić, T., Korać, A., Korać, B.,& Janković, A.. (2023). Nrf2 coordinates redox-metabolic homeostasis required for lipid deposition in rat visceral adipose tissue during the re-acclimation of rats after cold. in Redox Biology Congress 2023; 2023 Jun 6-9; Vienna, Austria
Elsevier., 26.
https://doi.org/10.1016/j.freeradbiomed.2023.03.183

Budnar Šoškić M, Zakić T, Korać A, Korać B, Janković A. Nrf2 coordinates redox-metabolic homeostasis required for lipid deposition in rat visceral adipose tissue during the re-acclimation of rats after cold. in Redox Biology Congress 2023; 2023 Jun 6-9; Vienna, Austria. 2023;:26.
doi:10.1016/j.freeradbiomed.2023.03.183 .

Budnar Šoškić, Marta, Zakić, Tamara, Korać, Aleksandra, Korać, Bato, Janković, Aleksandra, "Nrf2 coordinates redox-metabolic homeostasis required for lipid deposition in rat visceral adipose tissue during the re-acclimation of rats after cold" in Redox Biology Congress 2023; 2023 Jun 6-9; Vienna, Austria (2023):26,
https://doi.org/10.1016/j.freeradbiomed.2023.03.183 . .

TY  - JOUR
AU  - Zakić, Tamara
AU  - Peković-Vaughan, Vanja
AU  - Čvoro, Aleksandra
AU  - Korać, Aleksandra
AU  - Janković, Aleksandra
AU  - Korać, Bato
PY  - 2023
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6519
AB  - Redox and metabolic processes are tightly coupled in both physiological and pathological conditions. In cancer, their integration occurs at multiple levels and is characterized by synchronized reprogramming both in the tumor tissue and its specific but heterogeneous microenvironment. In breast cancer, the principal microenvironment is the cancer-associated adipose tissue (CAAT). Understanding how the redox-metabolic reprogramming becomes coordinated in human breast cancer is imperative both for cancer prevention and for the establishment of new therapeutic approaches. This review aims to provide an overview of the current knowledge of the redox profiles and regulation of intermediary metabolism in breast cancer while considering the tumor and CAAT of breast cancer as a unique Warburg's pseudo-organ. As cancer is now recognized as a systemic metabolic disease, we have paid particular attention to the cell-specific redox-metabolic reprogramming and the roles of estrogen receptors and circadian rhythms, as well as their crosstalk in the development, growth, progression, and prognosis of breast cancer.
PB  - John Wiley
T2  - FEBS Letters
T1  - Redox and metabolic reprogramming in breast cancer and cancer-associated adipose tissue
DO  - 10.1002/1873-3468.14794
ER  - 

@article{
author = "Zakić, Tamara and Peković-Vaughan, Vanja and Čvoro, Aleksandra and Korać, Aleksandra and Janković, Aleksandra and Korać, Bato",
year = "2023",
abstract = "Redox and metabolic processes are tightly coupled in both physiological and pathological conditions. In cancer, their integration occurs at multiple levels and is characterized by synchronized reprogramming both in the tumor tissue and its specific but heterogeneous microenvironment. In breast cancer, the principal microenvironment is the cancer-associated adipose tissue (CAAT). Understanding how the redox-metabolic reprogramming becomes coordinated in human breast cancer is imperative both for cancer prevention and for the establishment of new therapeutic approaches. This review aims to provide an overview of the current knowledge of the redox profiles and regulation of intermediary metabolism in breast cancer while considering the tumor and CAAT of breast cancer as a unique Warburg's pseudo-organ. As cancer is now recognized as a systemic metabolic disease, we have paid particular attention to the cell-specific redox-metabolic reprogramming and the roles of estrogen receptors and circadian rhythms, as well as their crosstalk in the development, growth, progression, and prognosis of breast cancer.",
publisher = "John Wiley",
journal = "FEBS Letters",
title = "Redox and metabolic reprogramming in breast cancer and cancer-associated adipose tissue",
doi = "10.1002/1873-3468.14794"
}

Zakić, T., Peković-Vaughan, V., Čvoro, A., Korać, A., Janković, A.,& Korać, B.. (2023). Redox and metabolic reprogramming in breast cancer and cancer-associated adipose tissue. in FEBS Letters
John Wiley..
https://doi.org/10.1002/1873-3468.14794

Zakić T, Peković-Vaughan V, Čvoro A, Korać A, Janković A, Korać B. Redox and metabolic reprogramming in breast cancer and cancer-associated adipose tissue. in FEBS Letters. 2023;.
doi:10.1002/1873-3468.14794 .

Zakić, Tamara, Peković-Vaughan, Vanja, Čvoro, Aleksandra, Korać, Aleksandra, Janković, Aleksandra, Korać, Bato, "Redox and metabolic reprogramming in breast cancer and cancer-associated adipose tissue" in FEBS Letters (2023),
https://doi.org/10.1002/1873-3468.14794 . .

TY  - JOUR
AU  - Zakić, Tamara
AU  - Stojanović, Sara
AU  - Janković, Aleksandra
AU  - Korać, Aleksandra
AU  - Peković‐Vaughan, Vanja
AU  - Korać, Bato
PY  - 2022
UR  - https://onlinelibrary.wiley.com/doi/10.1002/biof.1931
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5385
AB  - Adaptive responses to environmental and physiological challenges, including exposure to low environmental temperature, require extensive structural, redox, and metabolic reprogramming. Detailed molecular mechanisms of such processes in the skin are lacking, especially the role of nuclear factor erythroid 2-related factor 2 (Nrf2) and other closely related redox-sensitive transcription factors Nrf1, Nrf3, and nuclear respiratory factor (NRF1). To investigate the role of Nrf2, we examined redox and metabolic responses in the skin of wild-type (WT) mice and mice lacking functional Nrf2 (Nrf2 KO) at room (RT, 24 ± 1°C) and cold (4 ± 1°C) temperature. Our results demonstrate distinct expression profiles of major enzymes involved in antioxidant defense and key metabolic and mitochondrial pathways in the skin, depending on the functional Nrf2 and/or cold stimulus. Nrf2 KO mice at RT displayed profound alterations in redox, mitochondrial and metabolic responses, generally akin to cold-induced skin responses in WT mice. Immunohistochemical analyses of skin cell compartments (keratinocytes, fibroblasts, hair follicle, and sebaceous gland) and spatial locations (nucleus and cytoplasm) revealed synergistic interactions between members of the Nrf transcription factor family as part of redox-metabolic reprogramming in WT mice upon cold acclimation. In contrast, Nrf2 KO mice at RT showed loss of NRF1 expression and a compensatory activation of Nrf1/Nrf3, which was abolished upon cold, concomitant with blunted redox-metabolic responses. These data show for the first time a novel role for Nrf2 in skin physiology in response to low environmental temperature, with important implications in human connective tissue diseases with altered thermogenic responses.
T2  - BioFactors
T1  - Redox‐metabolic reprogramming of skin in mice lacking functional Nrf2 under basal conditions and cold acclimation
DO  - 10.1002/biof.1931
ER  - 

@article{
author = "Zakić, Tamara and Stojanović, Sara and Janković, Aleksandra and Korać, Aleksandra and Peković‐Vaughan, Vanja and Korać, Bato",
year = "2022",
abstract = "Adaptive responses to environmental and physiological challenges, including exposure to low environmental temperature, require extensive structural, redox, and metabolic reprogramming. Detailed molecular mechanisms of such processes in the skin are lacking, especially the role of nuclear factor erythroid 2-related factor 2 (Nrf2) and other closely related redox-sensitive transcription factors Nrf1, Nrf3, and nuclear respiratory factor (NRF1). To investigate the role of Nrf2, we examined redox and metabolic responses in the skin of wild-type (WT) mice and mice lacking functional Nrf2 (Nrf2 KO) at room (RT, 24 ± 1°C) and cold (4 ± 1°C) temperature. Our results demonstrate distinct expression profiles of major enzymes involved in antioxidant defense and key metabolic and mitochondrial pathways in the skin, depending on the functional Nrf2 and/or cold stimulus. Nrf2 KO mice at RT displayed profound alterations in redox, mitochondrial and metabolic responses, generally akin to cold-induced skin responses in WT mice. Immunohistochemical analyses of skin cell compartments (keratinocytes, fibroblasts, hair follicle, and sebaceous gland) and spatial locations (nucleus and cytoplasm) revealed synergistic interactions between members of the Nrf transcription factor family as part of redox-metabolic reprogramming in WT mice upon cold acclimation. In contrast, Nrf2 KO mice at RT showed loss of NRF1 expression and a compensatory activation of Nrf1/Nrf3, which was abolished upon cold, concomitant with blunted redox-metabolic responses. These data show for the first time a novel role for Nrf2 in skin physiology in response to low environmental temperature, with important implications in human connective tissue diseases with altered thermogenic responses.",
journal = "BioFactors",
title = "Redox‐metabolic reprogramming of skin in mice lacking functional Nrf2 under basal conditions and cold acclimation",
doi = "10.1002/biof.1931"
}

Zakić, T., Stojanović, S., Janković, A., Korać, A., Peković‐Vaughan, V.,& Korać, B.. (2022). Redox‐metabolic reprogramming of skin in mice lacking functional Nrf2 under basal conditions and cold acclimation. in BioFactors.
https://doi.org/10.1002/biof.1931

Zakić T, Stojanović S, Janković A, Korać A, Peković‐Vaughan V, Korać B. Redox‐metabolic reprogramming of skin in mice lacking functional Nrf2 under basal conditions and cold acclimation. in BioFactors. 2022;.
doi:10.1002/biof.1931 .

Zakić, Tamara, Stojanović, Sara, Janković, Aleksandra, Korać, Aleksandra, Peković‐Vaughan, Vanja, Korać, Bato, "Redox‐metabolic reprogramming of skin in mice lacking functional Nrf2 under basal conditions and cold acclimation" in BioFactors (2022),
https://doi.org/10.1002/biof.1931 . .

TY  - CONF
AU  - Petrović, Anja
AU  - Bogojević, Desanka
AU  - Ivanović Matić, Svetlana
AU  - Martinović, Vesna
AU  - Korać, Aleksandra
AU  - Jovanović Stojanov, Sofija
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2018
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5237
AB  - Oxidative stress through changes in antioxidative enzyme activities, glutathione metabolism and lipid peroxidation, leads to cell damage and even cell death. These changes are integrated in the pathogenetic mechanisms of the long-term, specific complications of diabetes, such as neuropathy, retinopathy, cardiomyopathy, nephropathy and hepatopathy. Recent studies have shed light on new redox sensitive endogenous targets which are important regulators of oxidative stress-induced damage. HMGB1 is a nuclear chaperone with an inflammatory function when released in the extracellular space. Extracellular HMGB1, through interaction with TLR4 receptors in its oxidized state, and with RAGE in its reduced state, controls the equilibrium between apoptosis and autophagy. HMGB1 is  a redox sensitive protein with a potentially harmful role. We therefore analyzed the changes in HMGB1 regulated signaling pathways by immunoprecipitation and Western blot that can lead to cell death or cell survival in the liver of streptozotocin (STZ)-induced diabetic rats during decreased oxidative stress after melatonin administration, and when HMGB1 release was inhibited by ethyl pyruvate. Inhibition of HMGB1 release decreased both apoptosis and autophagy, and supported the unchanged state in liver cells in STZ-treated rats as compared to the control animals. The decrease in oxidative stress achieved with melatonin decreased HMGB1 driven apoptosis but upregulated HMGB1 regulated protective autophagy, mitophagy in particular as the second level of antioxidative defense which was detected by electron microscopy. It provided a selective advantage, minimizing oxidant insults when primary antioxidant activities are compromised during oxidative stress. This adaptation led to improved cell survival in the liver of STZ-treated rats. These results showed that modulation of the role of HMGB1 in the extracellular space that was achieved by a decrease in oxidative stress is more desirable than complete inhibition of its release because HMGB1 has a protective role against oxidative injuries in diabetic liver.
PB  - Belgrade: Serbian Society for Mitochondrial and Free Radical Physiology
C3  - Book of Abstracts: Fourth Congress Challenges in Redox Biology: SSMFRP-2018; 2018 Sep 28-30; Belgrade, Serbia
T1  - The level of oxidative stress determines the role of extracellular HMGB1 protein in diabetic liver
SP  - 43
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5237
ER  - 

@conference{
author = "Petrović, Anja and Bogojević, Desanka and Ivanović Matić, Svetlana and Martinović, Vesna and Korać, Aleksandra and Jovanović Stojanov, Sofija and Poznanović, Goran and Grigorov, Ilijana",
year = "2018",
abstract = "Oxidative stress through changes in antioxidative enzyme activities, glutathione metabolism and lipid peroxidation, leads to cell damage and even cell death. These changes are integrated in the pathogenetic mechanisms of the long-term, specific complications of diabetes, such as neuropathy, retinopathy, cardiomyopathy, nephropathy and hepatopathy. Recent studies have shed light on new redox sensitive endogenous targets which are important regulators of oxidative stress-induced damage. HMGB1 is a nuclear chaperone with an inflammatory function when released in the extracellular space. Extracellular HMGB1, through interaction with TLR4 receptors in its oxidized state, and with RAGE in its reduced state, controls the equilibrium between apoptosis and autophagy. HMGB1 is  a redox sensitive protein with a potentially harmful role. We therefore analyzed the changes in HMGB1 regulated signaling pathways by immunoprecipitation and Western blot that can lead to cell death or cell survival in the liver of streptozotocin (STZ)-induced diabetic rats during decreased oxidative stress after melatonin administration, and when HMGB1 release was inhibited by ethyl pyruvate. Inhibition of HMGB1 release decreased both apoptosis and autophagy, and supported the unchanged state in liver cells in STZ-treated rats as compared to the control animals. The decrease in oxidative stress achieved with melatonin decreased HMGB1 driven apoptosis but upregulated HMGB1 regulated protective autophagy, mitophagy in particular as the second level of antioxidative defense which was detected by electron microscopy. It provided a selective advantage, minimizing oxidant insults when primary antioxidant activities are compromised during oxidative stress. This adaptation led to improved cell survival in the liver of STZ-treated rats. These results showed that modulation of the role of HMGB1 in the extracellular space that was achieved by a decrease in oxidative stress is more desirable than complete inhibition of its release because HMGB1 has a protective role against oxidative injuries in diabetic liver.",
publisher = "Belgrade: Serbian Society for Mitochondrial and Free Radical Physiology",
journal = "Book of Abstracts: Fourth Congress Challenges in Redox Biology: SSMFRP-2018; 2018 Sep 28-30; Belgrade, Serbia",
title = "The level of oxidative stress determines the role of extracellular HMGB1 protein in diabetic liver",
pages = "43",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5237"
}

Petrović, A., Bogojević, D., Ivanović Matić, S., Martinović, V., Korać, A., Jovanović Stojanov, S., Poznanović, G.,& Grigorov, I.. (2018). The level of oxidative stress determines the role of extracellular HMGB1 protein in diabetic liver. in Book of Abstracts: Fourth Congress Challenges in Redox Biology: SSMFRP-2018; 2018 Sep 28-30; Belgrade, Serbia
Belgrade: Serbian Society for Mitochondrial and Free Radical Physiology., 43.
https://hdl.handle.net/21.15107/rcub_ibiss_5237

Petrović A, Bogojević D, Ivanović Matić S, Martinović V, Korać A, Jovanović Stojanov S, Poznanović G, Grigorov I. The level of oxidative stress determines the role of extracellular HMGB1 protein in diabetic liver. in Book of Abstracts: Fourth Congress Challenges in Redox Biology: SSMFRP-2018; 2018 Sep 28-30; Belgrade, Serbia. 2018;:43.
https://hdl.handle.net/21.15107/rcub_ibiss_5237 .

Petrović, Anja, Bogojević, Desanka, Ivanović Matić, Svetlana, Martinović, Vesna, Korać, Aleksandra, Jovanović Stojanov, Sofija, Poznanović, Goran, Grigorov, Ilijana, "The level of oxidative stress determines the role of extracellular HMGB1 protein in diabetic liver" in Book of Abstracts: Fourth Congress Challenges in Redox Biology: SSMFRP-2018; 2018 Sep 28-30; Belgrade, Serbia (2018):43,
https://hdl.handle.net/21.15107/rcub_ibiss_5237 .

TY  - CONF
AU  - Petrović, Anja
AU  - Ivanović Matić, Svetlana
AU  - Bogojević, Desanka
AU  - Martinović, Vesna
AU  - Korać, Aleksandra
AU  - Jovanović Stojanov, Sofija
AU  - Stevanović, Jelena
AU  - Grigorov, Ilijana
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5244
AB  - Introduction: Hepatocellular death is the main trigger of liver disease. Since diabetic patients are very prone to liver diseases there is a urgent need to identify key regulators of cell death processes. High-mobility group box protein 1 (HMGB1) is a non-histone nuclear protein with a role in apoptotic and autophagic activation when it is present in cytosol and extracellular space. The aim of this study was to elucidate HMGB1 contribution to liver injury trough activation of apoptosis and autophagy in streptozotocin (STZ)-induced diabetic rats since the role of HMGB1 in hepatic cell death during diabetes is partially known. Methods: Diabetes was induced with a single intraperitoneal (i.p.) injection of STZ (65 mg/kg). Inhibition of HMGB1 release was achieved by ethyl pyruvate (80 mg/kg/i.p./daily). We followed changes in expression of serum and cytosolic HMGB1 and its interaction with TLR4 and RAGE and how these changes affect on apoptotic and autophagic activity and liver morphology. Results: In the serum of diabetic rats elevated levels of HMGB1 were accompanied by increased HMGB1 interactions with TLR4 and RAGE receptors. Enhancement in these interactions led to increased activity of both apoptotic and autophagic signaling pathways resulting in altered liver morphology and acummulation of autophagosomes in hepatocytes. Inhibition of HMGB1 release caused reduction in apoptotic and autophagic activity which resulted in preservation of normal liver architecture and decreased number of autophagosomes. Conclusion: HMGB1 causes liver damage through activation of apoptosis and autophagy, therefore it’s a suitable new target for prevention of liver diseases in diabetic patients.
PB  - Belgrade: University of Belgrade, Faculty of Biology
C3  - Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
T1  - Inhibition of HMGB1 release decreases both apoptopic and autophagic activity in the hepatocytes and reduce liver injury in streptozotocin treated rats
SP  - 65
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5244
ER  - 

@conference{
author = "Petrović, Anja and Ivanović Matić, Svetlana and Bogojević, Desanka and Martinović, Vesna and Korać, Aleksandra and Jovanović Stojanov, Sofija and Stevanović, Jelena and Grigorov, Ilijana",
year = "2017",
abstract = "Introduction: Hepatocellular death is the main trigger of liver disease. Since diabetic patients are very prone to liver diseases there is a urgent need to identify key regulators of cell death processes. High-mobility group box protein 1 (HMGB1) is a non-histone nuclear protein with a role in apoptotic and autophagic activation when it is present in cytosol and extracellular space. The aim of this study was to elucidate HMGB1 contribution to liver injury trough activation of apoptosis and autophagy in streptozotocin (STZ)-induced diabetic rats since the role of HMGB1 in hepatic cell death during diabetes is partially known. Methods: Diabetes was induced with a single intraperitoneal (i.p.) injection of STZ (65 mg/kg). Inhibition of HMGB1 release was achieved by ethyl pyruvate (80 mg/kg/i.p./daily). We followed changes in expression of serum and cytosolic HMGB1 and its interaction with TLR4 and RAGE and how these changes affect on apoptotic and autophagic activity and liver morphology. Results: In the serum of diabetic rats elevated levels of HMGB1 were accompanied by increased HMGB1 interactions with TLR4 and RAGE receptors. Enhancement in these interactions led to increased activity of both apoptotic and autophagic signaling pathways resulting in altered liver morphology and acummulation of autophagosomes in hepatocytes. Inhibition of HMGB1 release caused reduction in apoptotic and autophagic activity which resulted in preservation of normal liver architecture and decreased number of autophagosomes. Conclusion: HMGB1 causes liver damage through activation of apoptosis and autophagy, therefore it’s a suitable new target for prevention of liver diseases in diabetic patients.",
publisher = "Belgrade: University of Belgrade, Faculty of Biology",
journal = "Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.",
title = "Inhibition of HMGB1 release decreases both apoptopic and autophagic activity in the hepatocytes and reduce liver injury in streptozotocin treated rats",
pages = "65",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5244"
}

Petrović, A., Ivanović Matić, S., Bogojević, D., Martinović, V., Korać, A., Jovanović Stojanov, S., Stevanović, J.,& Grigorov, I.. (2017). Inhibition of HMGB1 release decreases both apoptopic and autophagic activity in the hepatocytes and reduce liver injury in streptozotocin treated rats. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
Belgrade: University of Belgrade, Faculty of Biology., 65.
https://hdl.handle.net/21.15107/rcub_ibiss_5244

Petrović A, Ivanović Matić S, Bogojević D, Martinović V, Korać A, Jovanović Stojanov S, Stevanović J, Grigorov I. Inhibition of HMGB1 release decreases both apoptopic and autophagic activity in the hepatocytes and reduce liver injury in streptozotocin treated rats. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.. 2017;:65.
https://hdl.handle.net/21.15107/rcub_ibiss_5244 .

Petrović, Anja, Ivanović Matić, Svetlana, Bogojević, Desanka, Martinović, Vesna, Korać, Aleksandra, Jovanović Stojanov, Sofija, Stevanović, Jelena, Grigorov, Ilijana, "Inhibition of HMGB1 release decreases both apoptopic and autophagic activity in the hepatocytes and reduce liver injury in streptozotocin treated rats" in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia. (2017):65,
https://hdl.handle.net/21.15107/rcub_ibiss_5244 .

TY  - JOUR
AU  - Hmaid, Amal AAA
AU  - Markelić, Milica
AU  - Otašević, Vesna
AU  - Mašović, Sava
AU  - Janković, Aleksandra
AU  - Korać, Bato
AU  - Korać, Aleksandra
PY  - 2016
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6212
AB  - Structural changes affecting cardiomyocyte function may contribute to the pathophysiological remodeling underlying cardiac function impairment. Recent reports have shown that endogenous nitric oxide (NO) plays an important role in this process. In order to examine the role of NO in cardiomyocyte remodeling, male rats were acclimated to room temperature (22 ± 1 °C) or cold (4 ± 1 °C) and treated with 2.25% l-arginine·HCl or 0.01% l-NAME (Nω-nitro-l-arginine methyl ester)·HCl for 45 days. Untreated groups served as controls. Right heart ventricles were routinely prepared for light microscopic examination. Stereological estimations of volume densities of cardiomyocytes, surrounding blood vessels and connective tissue, as well as the morphometric measurements of cardiomyocyte diameters were performed. Tissue sections were also analyzed for structural alterations. We observed that both l-arginine and l-NAME supplementation induced cardiomyocyte hypertrophy, regardless of ambient temperature. However, cardiomyocyte hypertrophy was associated with fibrosis and extra collagen deposition only in the l-NAME treated group. Taken together, our results suggest that NO has a modulatory role in right heart ventricle remodeling by coordinating hypertrophy of cardiomyocytes and fibrous tissue preventing cardiac fibrosis.
PB  - Elsevier
T2  - Saudi Journal of Biological Sciences
T1  - Structural alterations in rat myocardium induced by chronic l-arginine and l-NAME supplementation
IS  - 3
VL  - 25
DO  - 10.1016/j.sjbs.2016.01.022
SP  - 537
EP  - 544
ER  - 

@article{
author = "Hmaid, Amal AAA and Markelić, Milica and Otašević, Vesna and Mašović, Sava and Janković, Aleksandra and Korać, Bato and Korać, Aleksandra",
year = "2016",
abstract = "Structural changes affecting cardiomyocyte function may contribute to the pathophysiological remodeling underlying cardiac function impairment. Recent reports have shown that endogenous nitric oxide (NO) plays an important role in this process. In order to examine the role of NO in cardiomyocyte remodeling, male rats were acclimated to room temperature (22 ± 1 °C) or cold (4 ± 1 °C) and treated with 2.25% l-arginine·HCl or 0.01% l-NAME (Nω-nitro-l-arginine methyl ester)·HCl for 45 days. Untreated groups served as controls. Right heart ventricles were routinely prepared for light microscopic examination. Stereological estimations of volume densities of cardiomyocytes, surrounding blood vessels and connective tissue, as well as the morphometric measurements of cardiomyocyte diameters were performed. Tissue sections were also analyzed for structural alterations. We observed that both l-arginine and l-NAME supplementation induced cardiomyocyte hypertrophy, regardless of ambient temperature. However, cardiomyocyte hypertrophy was associated with fibrosis and extra collagen deposition only in the l-NAME treated group. Taken together, our results suggest that NO has a modulatory role in right heart ventricle remodeling by coordinating hypertrophy of cardiomyocytes and fibrous tissue preventing cardiac fibrosis.",
publisher = "Elsevier",
journal = "Saudi Journal of Biological Sciences",
title = "Structural alterations in rat myocardium induced by chronic l-arginine and l-NAME supplementation",
number = "3",
volume = "25",
doi = "10.1016/j.sjbs.2016.01.022",
pages = "537-544"
}

Hmaid, A. A., Markelić, M., Otašević, V., Mašović, S., Janković, A., Korać, B.,& Korać, A.. (2016). Structural alterations in rat myocardium induced by chronic l-arginine and l-NAME supplementation. in Saudi Journal of Biological Sciences
Elsevier., 25(3), 537-544.
https://doi.org/10.1016/j.sjbs.2016.01.022

Hmaid AA, Markelić M, Otašević V, Mašović S, Janković A, Korać B, Korać A. Structural alterations in rat myocardium induced by chronic l-arginine and l-NAME supplementation. in Saudi Journal of Biological Sciences. 2016;25(3):537-544.
doi:10.1016/j.sjbs.2016.01.022 .

Hmaid, Amal AAA, Markelić, Milica, Otašević, Vesna, Mašović, Sava, Janković, Aleksandra, Korać, Bato, Korać, Aleksandra, "Structural alterations in rat myocardium induced by chronic l-arginine and l-NAME supplementation" in Saudi Journal of Biological Sciences, 25, no. 3 (2016):537-544,
https://doi.org/10.1016/j.sjbs.2016.01.022 . .

TY  - CONF
AU  - Vučetić, Milica
AU  - Markelić, Milica
AU  - Janković, Aleksandra
AU  - Stančić, Ana
AU  - Otašević, Vesna
AU  - Korać, Aleksandra
AU  - Buzadžić, Biljana J.
AU  - Korać, Bato
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1910
AB  - Natural hypothermia, in addition to allowing energy saving in hostile conditions, has been associated with delayed aging and increased longevity. However, the molecular basis responsible for observed correlations between the use of daily torpor/hibernation and indices of rate of aging is hitherto unclear. Considering central role of mitochondria dysfunction in the ageing process, we examined several mechanisms that might be involved in mitochondrial protection against oxidative damage during euthermia-hypothermia (and vice versa) transition, in brown adipose tissue (BAT) of the European Ground Squirrel (Spermophilus citellus).

Results showed that in hibernation increased protein expression of Mn superoxide dismutase coincides with decreased content of ATP synthase and uncoupling protein 1. This suggests that BAT mitochondria during hibernation are protected from oxidative injuries by suppressed oxidative capacity, as well as by upregulated antioxidant defense. Also, the data indicate that such molecular pattern of changes is initiated already during prehibernating period. Namely, in this period we observed accumulations of hypoxia-inducible factor-1α (HIF-1α) and nuclear factor (erythroid 2-related)-like 2, which are probably responsible for suppressed oxidative metabolism, i.e. increased antioxidant capacity, respectively. Increased expression of the mitofusin 1 and detection of the megamitochondria in the prehibernating period indicate intensive mitofusion process in the BAT. This may be another mechanism of protection of mitochondrial content/function during euthermia-hypothermia transition.

The results of the study suggest mechanisms that might be associated with increased resistance of “hibernating” mitochondria to the oxidative damage. Also, the data showed that biochemistry responsible for redox balance within the cell involves integration of antioxidant response and transcription control of overall metabolism. Finally, the results go in favor of the previous reports that suggested HIF-1 as a negative modulator of aging.
PB  - Elsevier
C3  - SFRR-E/SNFS Conference Abstracts; 2015 Sep 1-4; Stuttgart, Germany
T1  - Molecular mechanisms of mitochondrial protection against oxidative
 damage in hibernators - the anti-aging effects of heterothermy
IS  - 1
VL  - 86
DO  - 10.1016/j.freeradbiomed.2015.07.028
ER  - 

@conference{
author = "Vučetić, Milica and Markelić, Milica and Janković, Aleksandra and Stančić, Ana and Otašević, Vesna and Korać, Aleksandra and Buzadžić, Biljana J. and Korać, Bato",
year = "2015",
abstract = "Natural hypothermia, in addition to allowing energy saving in hostile conditions, has been associated with delayed aging and increased longevity. However, the molecular basis responsible for observed correlations between the use of daily torpor/hibernation and indices of rate of aging is hitherto unclear. Considering central role of mitochondria dysfunction in the ageing process, we examined several mechanisms that might be involved in mitochondrial protection against oxidative damage during euthermia-hypothermia (and vice versa) transition, in brown adipose tissue (BAT) of the European Ground Squirrel (Spermophilus citellus).

Results showed that in hibernation increased protein expression of Mn superoxide dismutase coincides with decreased content of ATP synthase and uncoupling protein 1. This suggests that BAT mitochondria during hibernation are protected from oxidative injuries by suppressed oxidative capacity, as well as by upregulated antioxidant defense. Also, the data indicate that such molecular pattern of changes is initiated already during prehibernating period. Namely, in this period we observed accumulations of hypoxia-inducible factor-1α (HIF-1α) and nuclear factor (erythroid 2-related)-like 2, which are probably responsible for suppressed oxidative metabolism, i.e. increased antioxidant capacity, respectively. Increased expression of the mitofusin 1 and detection of the megamitochondria in the prehibernating period indicate intensive mitofusion process in the BAT. This may be another mechanism of protection of mitochondrial content/function during euthermia-hypothermia transition.

The results of the study suggest mechanisms that might be associated with increased resistance of “hibernating” mitochondria to the oxidative damage. Also, the data showed that biochemistry responsible for redox balance within the cell involves integration of antioxidant response and transcription control of overall metabolism. Finally, the results go in favor of the previous reports that suggested HIF-1 as a negative modulator of aging.",
publisher = "Elsevier",
journal = "SFRR-E/SNFS Conference Abstracts; 2015 Sep 1-4; Stuttgart, Germany",
title = "Molecular mechanisms of mitochondrial protection against oxidative
 damage in hibernators - the anti-aging effects of heterothermy",
number = "1",
volume = "86",
doi = "10.1016/j.freeradbiomed.2015.07.028"
}

Vučetić, M., Markelić, M., Janković, A., Stančić, A., Otašević, V., Korać, A., Buzadžić, B. J.,& Korać, B.. (2015). Molecular mechanisms of mitochondrial protection against oxidative
 damage in hibernators - the anti-aging effects of heterothermy. in SFRR-E/SNFS Conference Abstracts; 2015 Sep 1-4; Stuttgart, Germany
Elsevier., 86(1).
https://doi.org/10.1016/j.freeradbiomed.2015.07.028

Vučetić M, Markelić M, Janković A, Stančić A, Otašević V, Korać A, Buzadžić BJ, Korać B. Molecular mechanisms of mitochondrial protection against oxidative
 damage in hibernators - the anti-aging effects of heterothermy. in SFRR-E/SNFS Conference Abstracts; 2015 Sep 1-4; Stuttgart, Germany. 2015;86(1).
doi:10.1016/j.freeradbiomed.2015.07.028 .

Vučetić, Milica, Markelić, Milica, Janković, Aleksandra, Stančić, Ana, Otašević, Vesna, Korać, Aleksandra, Buzadžić, Biljana J., Korać, Bato, "Molecular mechanisms of mitochondrial protection against oxidative
 damage in hibernators - the anti-aging effects of heterothermy" in SFRR-E/SNFS Conference Abstracts; 2015 Sep 1-4; Stuttgart, Germany, 86, no. 1 (2015),
https://doi.org/10.1016/j.freeradbiomed.2015.07.028 . .

TY  - CONF
AU  - Petrović, Anja
AU  - Bogojević, Desanka
AU  - Ivanović-Matić, Svetlana
AU  - Martinović, Vesna
AU  - Korać, Aleksandra
AU  - Jovanović-Stojanov, Sofija
AU  - Stevanović, Jelena
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2015
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5654
AB  - Autophagy is a cellular process that involves lysosomal degradation and recycling of intracellular
organelles and proteins. By removing damaged and dysfunctional cellular components in order to
maintain energy homeostasis during cellular stress, autophagy can serve as a cytoprotective
mechanism. Also, it could lead to cell death if it‟s overactive or defective. Molecular mechanisms
responsible for the two faces of autophagy are still partially known. Therefore, for the development of
therapy based on autophagy modulation, it‟s necessary to fully define these processes. This study
investigated the role of oxidative stress on autophagic processes in the liver of diabetic rats and effects
of melatonin, as an antioxidant, on autophagy initiation/modulation. The liver, as one of the main
target organs of insulin, takes an important role in regulation of glucose homeostasis. In diabetes,
hypoinsulinemia followed by hyperglycemia increases mitochondrial proton gradient within the cells.
In this state organelles become the source of reactive oxidative species leading to macromolecule
damage which may cause necrotic, apoptotic or autophagic cell death. In the liver of diabetic rats
obtained four weeks after diabetes induction with streptozotocin (65 mg/kg, i.p.), light and electron
transmission microscopy showed significant changes in the structure of the cells and a large number of
necrotic cells. By using Western blot, immunoprecipitation and confocal microscopy analyses,
autophagy in diabetic liver was confirmed by increased expression of proteins required for
autophagosome formation, LC3B and Beclin1, and by the presence of Beclin1 interactions with its
activator HMGB1. In the state of oxidative stress HMGB1 is relocated from the nucleus to the
cytoplasm. Continuous melatonin treatment of diabetic rats (2mg/kg/daily, i.p.) leads to significant
reduction of liver damage, presumably through elevated mitochondrial autophagy. Melatonin
additionally contributes to elevated expression of LC3B and Beclin1, HMGB1-Beclin1 interactions
and autophagosome formation. Thus, it seems that melatonin protects the liver from diabetes induced
damage by favoring autophagy as a protective mechanism.
PB  - Belgrade : Serbian Society for Mitochondrial and Free-Radical Physiology
C3  - Book of Abstracts: Third Congress Redox Medicine: Reactive Species Signaling, Analytical Methods, Phytopharmacy, Molecular Mechanisms of Disease - SSMFRP-2015; 2015 Sep 25-26; Belgrade, Serbia
T1  - Effects of melatonin on autophagic processes in the liver of diabetic rats
SP  - 33
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5654
ER  - 

@conference{
author = "Petrović, Anja and Bogojević, Desanka and Ivanović-Matić, Svetlana and Martinović, Vesna and Korać, Aleksandra and Jovanović-Stojanov, Sofija and Stevanović, Jelena and Poznanović, Goran and Grigorov, Ilijana",
year = "2015",
abstract = "Autophagy is a cellular process that involves lysosomal degradation and recycling of intracellular
organelles and proteins. By removing damaged and dysfunctional cellular components in order to
maintain energy homeostasis during cellular stress, autophagy can serve as a cytoprotective
mechanism. Also, it could lead to cell death if it‟s overactive or defective. Molecular mechanisms
responsible for the two faces of autophagy are still partially known. Therefore, for the development of
therapy based on autophagy modulation, it‟s necessary to fully define these processes. This study
investigated the role of oxidative stress on autophagic processes in the liver of diabetic rats and effects
of melatonin, as an antioxidant, on autophagy initiation/modulation. The liver, as one of the main
target organs of insulin, takes an important role in regulation of glucose homeostasis. In diabetes,
hypoinsulinemia followed by hyperglycemia increases mitochondrial proton gradient within the cells.
In this state organelles become the source of reactive oxidative species leading to macromolecule
damage which may cause necrotic, apoptotic or autophagic cell death. In the liver of diabetic rats
obtained four weeks after diabetes induction with streptozotocin (65 mg/kg, i.p.), light and electron
transmission microscopy showed significant changes in the structure of the cells and a large number of
necrotic cells. By using Western blot, immunoprecipitation and confocal microscopy analyses,
autophagy in diabetic liver was confirmed by increased expression of proteins required for
autophagosome formation, LC3B and Beclin1, and by the presence of Beclin1 interactions with its
activator HMGB1. In the state of oxidative stress HMGB1 is relocated from the nucleus to the
cytoplasm. Continuous melatonin treatment of diabetic rats (2mg/kg/daily, i.p.) leads to significant
reduction of liver damage, presumably through elevated mitochondrial autophagy. Melatonin
additionally contributes to elevated expression of LC3B and Beclin1, HMGB1-Beclin1 interactions
and autophagosome formation. Thus, it seems that melatonin protects the liver from diabetes induced
damage by favoring autophagy as a protective mechanism.",
publisher = "Belgrade : Serbian Society for Mitochondrial and Free-Radical Physiology",
journal = "Book of Abstracts: Third Congress Redox Medicine: Reactive Species Signaling, Analytical Methods, Phytopharmacy, Molecular Mechanisms of Disease - SSMFRP-2015; 2015 Sep 25-26; Belgrade, Serbia",
title = "Effects of melatonin on autophagic processes in the liver of diabetic rats",
pages = "33",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5654"
}

Petrović, A., Bogojević, D., Ivanović-Matić, S., Martinović, V., Korać, A., Jovanović-Stojanov, S., Stevanović, J., Poznanović, G.,& Grigorov, I.. (2015). Effects of melatonin on autophagic processes in the liver of diabetic rats. in Book of Abstracts: Third Congress Redox Medicine: Reactive Species Signaling, Analytical Methods, Phytopharmacy, Molecular Mechanisms of Disease - SSMFRP-2015; 2015 Sep 25-26; Belgrade, Serbia
Belgrade : Serbian Society for Mitochondrial and Free-Radical Physiology., 33.
https://hdl.handle.net/21.15107/rcub_ibiss_5654

Petrović A, Bogojević D, Ivanović-Matić S, Martinović V, Korać A, Jovanović-Stojanov S, Stevanović J, Poznanović G, Grigorov I. Effects of melatonin on autophagic processes in the liver of diabetic rats. in Book of Abstracts: Third Congress Redox Medicine: Reactive Species Signaling, Analytical Methods, Phytopharmacy, Molecular Mechanisms of Disease - SSMFRP-2015; 2015 Sep 25-26; Belgrade, Serbia. 2015;:33.
https://hdl.handle.net/21.15107/rcub_ibiss_5654 .

Petrović, Anja, Bogojević, Desanka, Ivanović-Matić, Svetlana, Martinović, Vesna, Korać, Aleksandra, Jovanović-Stojanov, Sofija, Stevanović, Jelena, Poznanović, Goran, Grigorov, Ilijana, "Effects of melatonin on autophagic processes in the liver of diabetic rats" in Book of Abstracts: Third Congress Redox Medicine: Reactive Species Signaling, Analytical Methods, Phytopharmacy, Molecular Mechanisms of Disease - SSMFRP-2015; 2015 Sep 25-26; Belgrade, Serbia (2015):33,
https://hdl.handle.net/21.15107/rcub_ibiss_5654 .

TY  - JOUR
AU  - Janković, Aleksandra
AU  - Korac, Aleksandra
AU  - Buzadžić, Biljana J.
AU  - Otašević, Vesna
AU  - Stančić, Ana
AU  - Daiber, Andreas
AU  - Korać, Bato
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2326
AB  - Obesity is an energy balance disorder associated with dyslipidemia,
   insulin resistance and diabetes type 2, also summarized with the term
   metabolic syndrome or syndrome X. Increasing evidence points to
   ``adipocyte dysfunction{''}, rather than fat mass accretion per se, as
   the key pathophysiological factor for metabolic complications in
   obesity. The dysfunctional fat tissue in obesity characterizes a failure
   to safely store metabolic substrates into existing hypertrophied
   adipocytes and/or into new preadipocytes recruited for differentiation.
   In this review we briefly summarize the potential of redox imbalance in
   fat tissue as an instigator of adipocyte dysfunction in obesity. We
   reveal the challenge of the adipose redox changes, insights in the
   regulation of healthy expansion of adipose tissue and its reduction,
   leading to glucose and lipids overflow. (C) 2015 Published by Elsevier
   B.V.
T2  - Redox Biology
T1  - Redox implications in adipose tissue (dys)function-A new look at old
 acquaintances
VL  - 6
DO  - 10.1016/j.redox.2015.06.018
SP  - 19
EP  - 32
ER  - 

@article{
author = "Janković, Aleksandra and Korac, Aleksandra and Buzadžić, Biljana J. and Otašević, Vesna and Stančić, Ana and Daiber, Andreas and Korać, Bato",
year = "2015",
abstract = "Obesity is an energy balance disorder associated with dyslipidemia,
   insulin resistance and diabetes type 2, also summarized with the term
   metabolic syndrome or syndrome X. Increasing evidence points to
   ``adipocyte dysfunction{''}, rather than fat mass accretion per se, as
   the key pathophysiological factor for metabolic complications in
   obesity. The dysfunctional fat tissue in obesity characterizes a failure
   to safely store metabolic substrates into existing hypertrophied
   adipocytes and/or into new preadipocytes recruited for differentiation.
   In this review we briefly summarize the potential of redox imbalance in
   fat tissue as an instigator of adipocyte dysfunction in obesity. We
   reveal the challenge of the adipose redox changes, insights in the
   regulation of healthy expansion of adipose tissue and its reduction,
   leading to glucose and lipids overflow. (C) 2015 Published by Elsevier
   B.V.",
journal = "Redox Biology",
title = "Redox implications in adipose tissue (dys)function-A new look at old
 acquaintances",
volume = "6",
doi = "10.1016/j.redox.2015.06.018",
pages = "19-32"
}

Janković, A., Korac, A., Buzadžić, B. J., Otašević, V., Stančić, A., Daiber, A.,& Korać, B.. (2015). Redox implications in adipose tissue (dys)function-A new look at old
 acquaintances. in Redox Biology, 6, 19-32.
https://doi.org/10.1016/j.redox.2015.06.018

Janković A, Korac A, Buzadžić BJ, Otašević V, Stančić A, Daiber A, Korać B. Redox implications in adipose tissue (dys)function-A new look at old
 acquaintances. in Redox Biology. 2015;6:19-32.
doi:10.1016/j.redox.2015.06.018 .

Janković, Aleksandra, Korac, Aleksandra, Buzadžić, Biljana J., Otašević, Vesna, Stančić, Ana, Daiber, Andreas, Korać, Bato, "Redox implications in adipose tissue (dys)function-A new look at old
 acquaintances" in Redox Biology, 6 (2015):19-32,
https://doi.org/10.1016/j.redox.2015.06.018 . .

TY  - JOUR
AU  - Janković, Aleksandra
AU  - Golic, Igor
AU  - Markelic, Milica
AU  - Stančić, Ana
AU  - Otašević, Vesna
AU  - Buzadžić, Biljana J.
AU  - Korac, Aleksandra
AU  - Korać, Bato
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1921
AB  - Conversion of white into brown adipose tissue may have important
   implications in obesity resistance and treatment. Several browning
   agents or conditions ignite thermogenesis in white adipose tissue (WAT).
   To reveal the capacity of WAT to function in a brownish/burning mode
   over the long term, we investigated the progression of the rat
   retroperitoneal WAT (rpWAT) browning during 45days of cold acclimation.
   During the early stages of cold acclimation, the majority of rpWAT
   adipocytes underwent multilocularization and thermogenic-profile
   induction, as demonstrated by the presence of a multitude of uncoupling
   protein 1 (UCP1)-immunopositive paucilocular adipocytes containing
   peroxisome proliferator-activated receptor (PPAR) coactivator-1 (PGC-1)
   and PR domain-containing 16 (PRDM16) in their nuclei. After 45days, all
   adipocytes remained PRDM16 immunopositive, but only a few multilocular
   adipocytes rich in mitochondria remained UCP1/PGC-1 immunopositive.
   Molecular evidence showed that thermogenic recruitment of rpWAT occurred
   following cold exposure, but returned to starting levels after cold
   acclimation. Compared with controls (22 +/- 1 degrees C), levels of UCP1
   mRNA increased in parallel with PPAR (PPAR from days 1 to 7 and PGC-1 on
   day 1). Transcriptional recruitment of rpWAT was followed by an increase
   in UCP1 protein content (from days 1 to 21). Results clearly showed that
   most of the adipocytes within rpWAT underwent transient brown-fat-like
   thermogenic recruitment upon stimulation, but only a minority of cells
   retained a brown adipose tissue-like phenotype after the attainment of
   cold acclimation. Therefore, browning of WAT is dependent on both
   maintaining the thermogenic response and retaining enough brown-like
   thermogenically competent adipocytes in the long-term. Both aspects of
   browning could be important for long-term energy homeostasis and
   body-weight regulation.
T2  - Journal of Physiology-London
T1  - Two key temporally distinguishable molecular and cellular components of
 white adipose tissue browning during cold acclimation
IS  - 15
VL  - 593
DO  - 10.1113/JP270805
SP  - 3267
EP  - 3280
ER  - 

@article{
author = "Janković, Aleksandra and Golic, Igor and Markelic, Milica and Stančić, Ana and Otašević, Vesna and Buzadžić, Biljana J. and Korac, Aleksandra and Korać, Bato",
year = "2015",
abstract = "Conversion of white into brown adipose tissue may have important
   implications in obesity resistance and treatment. Several browning
   agents or conditions ignite thermogenesis in white adipose tissue (WAT).
   To reveal the capacity of WAT to function in a brownish/burning mode
   over the long term, we investigated the progression of the rat
   retroperitoneal WAT (rpWAT) browning during 45days of cold acclimation.
   During the early stages of cold acclimation, the majority of rpWAT
   adipocytes underwent multilocularization and thermogenic-profile
   induction, as demonstrated by the presence of a multitude of uncoupling
   protein 1 (UCP1)-immunopositive paucilocular adipocytes containing
   peroxisome proliferator-activated receptor (PPAR) coactivator-1 (PGC-1)
   and PR domain-containing 16 (PRDM16) in their nuclei. After 45days, all
   adipocytes remained PRDM16 immunopositive, but only a few multilocular
   adipocytes rich in mitochondria remained UCP1/PGC-1 immunopositive.
   Molecular evidence showed that thermogenic recruitment of rpWAT occurred
   following cold exposure, but returned to starting levels after cold
   acclimation. Compared with controls (22 +/- 1 degrees C), levels of UCP1
   mRNA increased in parallel with PPAR (PPAR from days 1 to 7 and PGC-1 on
   day 1). Transcriptional recruitment of rpWAT was followed by an increase
   in UCP1 protein content (from days 1 to 21). Results clearly showed that
   most of the adipocytes within rpWAT underwent transient brown-fat-like
   thermogenic recruitment upon stimulation, but only a minority of cells
   retained a brown adipose tissue-like phenotype after the attainment of
   cold acclimation. Therefore, browning of WAT is dependent on both
   maintaining the thermogenic response and retaining enough brown-like
   thermogenically competent adipocytes in the long-term. Both aspects of
   browning could be important for long-term energy homeostasis and
   body-weight regulation.",
journal = "Journal of Physiology-London",
title = "Two key temporally distinguishable molecular and cellular components of
 white adipose tissue browning during cold acclimation",
number = "15",
volume = "593",
doi = "10.1113/JP270805",
pages = "3267-3280"
}

Janković, A., Golic, I., Markelic, M., Stančić, A., Otašević, V., Buzadžić, B. J., Korac, A.,& Korać, B.. (2015). Two key temporally distinguishable molecular and cellular components of
 white adipose tissue browning during cold acclimation. in Journal of Physiology-London, 593(15), 3267-3280.
https://doi.org/10.1113/JP270805

Janković A, Golic I, Markelic M, Stančić A, Otašević V, Buzadžić BJ, Korac A, Korać B. Two key temporally distinguishable molecular and cellular components of
 white adipose tissue browning during cold acclimation. in Journal of Physiology-London. 2015;593(15):3267-3280.
doi:10.1113/JP270805 .

Janković, Aleksandra, Golic, Igor, Markelic, Milica, Stančić, Ana, Otašević, Vesna, Buzadžić, Biljana J., Korac, Aleksandra, Korać, Bato, "Two key temporally distinguishable molecular and cellular components of
 white adipose tissue browning during cold acclimation" in Journal of Physiology-London, 593, no. 15 (2015):3267-3280,
https://doi.org/10.1113/JP270805 . .

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  - Bulatović, Mirna Z.
AU  - Maksimović-Ivanić, Danijela
AU  - Bensing, Christian
AU  - Gomez-Ruiz, Santiago
AU  - Steinborn, Dirk
AU  - Schmidt, Harry
AU  - Mojić, Marija
AU  - Korac, Aleksandra
AU  - Golic, Igor
AU  - Perez-Quintanilla, Damian
AU  - Momčilović, Miljana
AU  - Mijatović, Sanja
AU  - Kaluđerović, Goran N.
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2205
AB  - The strong therapeutic potential of an organotin(IV) compound loaded in
   nanostructured silica (SBA-15pSn) is demonstrated: B16 melanoma tumor
   growth in syngeneic C57BL/6 mice is almost completely abolished. In
   contrast to apoptosis as the basic mechanism of the anticancer action of
   numerous chemotherapeutics, the important advantage of this SBA-15pSn
   mesoporous material is the induction of cell differentiation, an effect
   unknown for metal-based drugs and nanomaterials alone. This
   non-aggressive mode of drug action is highly efficient against cancer
   cells but is in the concentration range used nontoxic for normal tissue.
   JNK (Jun-amino-terminal kinase)-independent apoptosis accompanied by the
   development of the melanocyte-like nonproliferative phenotype of
   survived cells indicates the extraordinary potential of SBA-15pSn to
   suppress tumor growth without undesirable compensatory proliferation of
   malignant cells in response to neighboring cell death.
T2  - Angewandte Chemie-International Edition
T1  - Organotin(IV)-Loaded Mesoporous Silica as a Biocompatible Strategy in
 Cancer Treatment
IS  - 23
VL  - 53
DO  - 10.1002/anie.201400763
SP  - 5982
EP  - 5987
ER  - 

@article{
author = "Bulatović, Mirna Z. and Maksimović-Ivanić, Danijela and Bensing, Christian and Gomez-Ruiz, Santiago and Steinborn, Dirk and Schmidt, Harry and Mojić, Marija and Korac, Aleksandra and Golic, Igor and Perez-Quintanilla, Damian and Momčilović, Miljana and Mijatović, Sanja and Kaluđerović, Goran N.",
year = "2014",
abstract = "The strong therapeutic potential of an organotin(IV) compound loaded in
   nanostructured silica (SBA-15pSn) is demonstrated: B16 melanoma tumor
   growth in syngeneic C57BL/6 mice is almost completely abolished. In
   contrast to apoptosis as the basic mechanism of the anticancer action of
   numerous chemotherapeutics, the important advantage of this SBA-15pSn
   mesoporous material is the induction of cell differentiation, an effect
   unknown for metal-based drugs and nanomaterials alone. This
   non-aggressive mode of drug action is highly efficient against cancer
   cells but is in the concentration range used nontoxic for normal tissue.
   JNK (Jun-amino-terminal kinase)-independent apoptosis accompanied by the
   development of the melanocyte-like nonproliferative phenotype of
   survived cells indicates the extraordinary potential of SBA-15pSn to
   suppress tumor growth without undesirable compensatory proliferation of
   malignant cells in response to neighboring cell death.",
journal = "Angewandte Chemie-International Edition",
title = "Organotin(IV)-Loaded Mesoporous Silica as a Biocompatible Strategy in
 Cancer Treatment",
number = "23",
volume = "53",
doi = "10.1002/anie.201400763",
pages = "5982-5987"
}

Bulatović, M. Z., Maksimović-Ivanić, D., Bensing, C., Gomez-Ruiz, S., Steinborn, D., Schmidt, H., Mojić, M., Korac, A., Golic, I., Perez-Quintanilla, D., Momčilović, M., Mijatović, S.,& Kaluđerović, G. N.. (2014). Organotin(IV)-Loaded Mesoporous Silica as a Biocompatible Strategy in
 Cancer Treatment. in Angewandte Chemie-International Edition, 53(23), 5982-5987.
https://doi.org/10.1002/anie.201400763

Bulatović MZ, Maksimović-Ivanić D, Bensing C, Gomez-Ruiz S, Steinborn D, Schmidt H, Mojić M, Korac A, Golic I, Perez-Quintanilla D, Momčilović M, Mijatović S, Kaluđerović GN. Organotin(IV)-Loaded Mesoporous Silica as a Biocompatible Strategy in
 Cancer Treatment. in Angewandte Chemie-International Edition. 2014;53(23):5982-5987.
doi:10.1002/anie.201400763 .

Bulatović, Mirna Z., Maksimović-Ivanić, Danijela, Bensing, Christian, Gomez-Ruiz, Santiago, Steinborn, Dirk, Schmidt, Harry, Mojić, Marija, Korac, Aleksandra, Golic, Igor, Perez-Quintanilla, Damian, Momčilović, Miljana, Mijatović, Sanja, Kaluđerović, Goran N., "Organotin(IV)-Loaded Mesoporous Silica as a Biocompatible Strategy in
 Cancer Treatment" in Angewandte Chemie-International Edition, 53, no. 23 (2014):5982-5987,
https://doi.org/10.1002/anie.201400763 . .

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 . .