TY  - JOUR
AU  - Stančić, Ana
AU  - Janković, Aleksandra
AU  - Korać, Aleksandra
AU  - Buzadžić, Biljana
AU  - Otašević, Vesna
AU  - Korać, Bato
PY  - 2018
UR  - http://linkinghub.elsevier.com/retrieve/pii/S0047637417301252
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2859
AB  - The role of nitric oxide (NO) in cutaneous physiology/pathology became a growing research field since the discovery that almost all types of skin cells can synthetize this redox signaling molecule about 20 years ago. Now, it is evident that NO is an important player in skin physiological processes and in responses of cutaneous cells to external insults, while the impaired NO signaling has an important consequence in skin pathology. Skin disorders are common complications in diabetic conditions. Various metabolic/biochemical and immunological dysregulations in diabetic skin are tightly coupled with the disturbances in the redox state, primarily the ratio between NO and superoxide (O(cyrillic) 2 - ). This review describes possible therapeutic significance of different redox state modulators in the treatment of diabetic skin disorders. The focus is on those modulators that tightly control NO/O(cyrillic) 2 - ratio through the complex mechanisms affecting endogenous NO and O(cyrillic) 2 - producing and removing systems. The fact that classic antioxidants failed to show significant benefits in diabetes, emphasizes the importance of such redox mechanism-based and targeted approaches.
T2  - Mechanisms of Ageing and Development
T1  - The role of nitric oxide in diabetic skin (patho)physiology
VL  - 172
DO  - 10.1016/j.mad.2017.08.018
SP  - 21
EP  - 29
ER  - 

@article{
author = "Stančić, Ana and Janković, Aleksandra and Korać, Aleksandra and Buzadžić, Biljana and Otašević, Vesna and Korać, Bato",
year = "2018",
abstract = "The role of nitric oxide (NO) in cutaneous physiology/pathology became a growing research field since the discovery that almost all types of skin cells can synthetize this redox signaling molecule about 20 years ago. Now, it is evident that NO is an important player in skin physiological processes and in responses of cutaneous cells to external insults, while the impaired NO signaling has an important consequence in skin pathology. Skin disorders are common complications in diabetic conditions. Various metabolic/biochemical and immunological dysregulations in diabetic skin are tightly coupled with the disturbances in the redox state, primarily the ratio between NO and superoxide (O(cyrillic) 2 - ). This review describes possible therapeutic significance of different redox state modulators in the treatment of diabetic skin disorders. The focus is on those modulators that tightly control NO/O(cyrillic) 2 - ratio through the complex mechanisms affecting endogenous NO and O(cyrillic) 2 - producing and removing systems. The fact that classic antioxidants failed to show significant benefits in diabetes, emphasizes the importance of such redox mechanism-based and targeted approaches.",
journal = "Mechanisms of Ageing and Development",
title = "The role of nitric oxide in diabetic skin (patho)physiology",
volume = "172",
doi = "10.1016/j.mad.2017.08.018",
pages = "21-29"
}

Stančić, A., Janković, A., Korać, A., Buzadžić, B., Otašević, V.,& Korać, B.. (2018). The role of nitric oxide in diabetic skin (patho)physiology. in Mechanisms of Ageing and Development, 172, 21-29.
https://doi.org/10.1016/j.mad.2017.08.018

Stančić A, Janković A, Korać A, Buzadžić B, Otašević V, Korać B. The role of nitric oxide in diabetic skin (patho)physiology. in Mechanisms of Ageing and Development. 2018;172:21-29.
doi:10.1016/j.mad.2017.08.018 .

Stančić, Ana, Janković, Aleksandra, Korać, Aleksandra, Buzadžić, Biljana, Otašević, Vesna, Korać, Bato, "The role of nitric oxide in diabetic skin (patho)physiology" in Mechanisms of Ageing and Development, 172 (2018):21-29,
https://doi.org/10.1016/j.mad.2017.08.018 . .

TY  - JOUR
AU  - Janković, Aleksandra
AU  - Korać, Aleksandra
AU  - Buzadžić, Biljana
AU  - Stančić, Ana
AU  - Otašević, Vesna
AU  - Ferdinandy, Peter
AU  - Daiber, Andreas
AU  - Korać, Bato
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6734
AB  - Insulin sensitivity and metabolic homeostasis depend on the capacity of adipose tissue to take up and utilize excess glucose and fatty acids. The key aspects that determine the fuel‐buffering capacity of adipose tissue depend on the physiological levels of the small redox molecule, nitric oxide (NO). In addition to impairment of NO synthesis, excessive formation of the superoxide anion (О2 •–) in adipose tissue may be an important interfering factor diverting the signalling of NO and other reactive oxygen and nitrogen species in obesity, resulting in metabolic dysfunction of adipose tissue over time. Besides its role in relief from superoxide burst, enhanced NO signalling may be responsible for the therapeutic benefits of different superoxide dismutase mimetics, in obesity and experimental diabetes models. This review summarizes the role of NO in adipose tissue and highlights the effects of NO/О2 •– ratio ‘teetering’ as a promising pharmacological target in the metabolic syndrome.
PB  - John Wiley & Sons, Inc
T2  - British Journal of Pharmacology
T1  - Targeting the NO/superoxide ratio in adipose tissue: relevance to obesity and diabetes management
IS  - 12
VL  - 174
DO  - 10.1111/bph.13498
SP  - 1570
EP  - 1590
ER  - 

@article{
author = "Janković, Aleksandra and Korać, Aleksandra and Buzadžić, Biljana and Stančić, Ana and Otašević, Vesna and Ferdinandy, Peter and Daiber, Andreas and Korać, Bato",
year = "2017",
abstract = "Insulin sensitivity and metabolic homeostasis depend on the capacity of adipose tissue to take up and utilize excess glucose and fatty acids. The key aspects that determine the fuel‐buffering capacity of adipose tissue depend on the physiological levels of the small redox molecule, nitric oxide (NO). In addition to impairment of NO synthesis, excessive formation of the superoxide anion (О2 •–) in adipose tissue may be an important interfering factor diverting the signalling of NO and other reactive oxygen and nitrogen species in obesity, resulting in metabolic dysfunction of adipose tissue over time. Besides its role in relief from superoxide burst, enhanced NO signalling may be responsible for the therapeutic benefits of different superoxide dismutase mimetics, in obesity and experimental diabetes models. This review summarizes the role of NO in adipose tissue and highlights the effects of NO/О2 •– ratio ‘teetering’ as a promising pharmacological target in the metabolic syndrome.",
publisher = "John Wiley & Sons, Inc",
journal = "British Journal of Pharmacology",
title = "Targeting the NO/superoxide ratio in adipose tissue: relevance to obesity and diabetes management",
number = "12",
volume = "174",
doi = "10.1111/bph.13498",
pages = "1570-1590"
}

Janković, A., Korać, A., Buzadžić, B., Stančić, A., Otašević, V., Ferdinandy, P., Daiber, A.,& Korać, B.. (2017). Targeting the NO/superoxide ratio in adipose tissue: relevance to obesity and diabetes management. in British Journal of Pharmacology
John Wiley & Sons, Inc., 174(12), 1570-1590.
https://doi.org/10.1111/bph.13498

Janković A, Korać A, Buzadžić B, Stančić A, Otašević V, Ferdinandy P, Daiber A, Korać B. Targeting the NO/superoxide ratio in adipose tissue: relevance to obesity and diabetes management. in British Journal of Pharmacology. 2017;174(12):1570-1590.
doi:10.1111/bph.13498 .

Janković, Aleksandra, Korać, Aleksandra, Buzadžić, Biljana, Stančić, Ana, Otašević, Vesna, Ferdinandy, Peter, Daiber, Andreas, Korać, Bato, "Targeting the NO/superoxide ratio in adipose tissue: relevance to obesity and diabetes management" in British Journal of Pharmacology, 174, no. 12 (2017):1570-1590,
https://doi.org/10.1111/bph.13498 . .

TY  - JOUR
AU  - Stančić, Ana
AU  - Filipović, Miloš
AU  - Ivanović-Burmazović, Ivana
AU  - Mašović, Sava
AU  - Janković, Aleksandra
AU  - Otašević, Vesna
AU  - Korać, Aleksandra
AU  - Buzadžić, Biljana
AU  - Korać, Bato
PY  - 2017
UR  - http://linkinghub.elsevier.com/retrieve/pii/S0009279717300030
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2766
AB  - Considering the vital role of skeletal muscle in control of whole-body metabolism and the severity of long-term diabetic complications, we aimed to reveal the molecular pattern of early diabetes-related skeletal muscle phenotype in terms of energy metabolism, focusing on regulatory mechanisms, and the possibility to improve it using two redox modulators, L-arginine and superoxide dismutase (SOD) mimic. Alloxan-induced diabetic rats (120 mg/kg) were treated with L-arginine or the highly specific SOD mimic, M40403, for 7 days. As appropriate controls, non-diabetic rats received the same treatments. We found that L-arginine and M40403 restored diabetes-induced impairment of phospho-5′-AMP-activated protein kinase α (AMPKα) signaling by upregulating AMPKα protein itself and its downstream effectors, peroxisome proliferator-activated receptor-γ coactivator-1α and nuclear respiratory factor 1. Also, there was a restitution of the protein levels of oxidative phosphorylation components (complex I, complex II and complex IV) and mitofusin 2. Furthermore, L-arginine and M40403 induced translocation of glucose transporter 4 to the membrane and upregulation of protein of phosphofructokinase and acyl coenzyme A dehydrogenase, diminishing negative diabetic effects on limiting factors of glucose and lipid metabolism. Both treatments abolished diabetes-induced downregulation of sarcoplasmic reticulum calcium-ATPase proteins (SERCA 1 and 2). Similar effects of L-arginine and SOD mimic treatments suggest that disturbances in the superoxide/nitric oxide ratio may be responsible for skeletal muscle mitochondrial and metabolic impairment in early diabetes. Our results provide evidence that L-arginine and SOD mimics have potential in preventing and treating metabolic disturbances accompanying this widespread metabolic disease.
T2  - Chemico-Biological Interactions
T1  - Early energy metabolism-related molecular events in skeletal muscle of diabetic rats: The effects of l -arginine and SOD mimic
VL  - 272
DO  - 10.1016/j.cbi.2017.05.003
SP  - 188
EP  - 196
ER  - 

@article{
author = "Stančić, Ana and Filipović, Miloš and Ivanović-Burmazović, Ivana and Mašović, Sava and Janković, Aleksandra and Otašević, Vesna and Korać, Aleksandra and Buzadžić, Biljana and Korać, Bato",
year = "2017",
abstract = "Considering the vital role of skeletal muscle in control of whole-body metabolism and the severity of long-term diabetic complications, we aimed to reveal the molecular pattern of early diabetes-related skeletal muscle phenotype in terms of energy metabolism, focusing on regulatory mechanisms, and the possibility to improve it using two redox modulators, L-arginine and superoxide dismutase (SOD) mimic. Alloxan-induced diabetic rats (120 mg/kg) were treated with L-arginine or the highly specific SOD mimic, M40403, for 7 days. As appropriate controls, non-diabetic rats received the same treatments. We found that L-arginine and M40403 restored diabetes-induced impairment of phospho-5′-AMP-activated protein kinase α (AMPKα) signaling by upregulating AMPKα protein itself and its downstream effectors, peroxisome proliferator-activated receptor-γ coactivator-1α and nuclear respiratory factor 1. Also, there was a restitution of the protein levels of oxidative phosphorylation components (complex I, complex II and complex IV) and mitofusin 2. Furthermore, L-arginine and M40403 induced translocation of glucose transporter 4 to the membrane and upregulation of protein of phosphofructokinase and acyl coenzyme A dehydrogenase, diminishing negative diabetic effects on limiting factors of glucose and lipid metabolism. Both treatments abolished diabetes-induced downregulation of sarcoplasmic reticulum calcium-ATPase proteins (SERCA 1 and 2). Similar effects of L-arginine and SOD mimic treatments suggest that disturbances in the superoxide/nitric oxide ratio may be responsible for skeletal muscle mitochondrial and metabolic impairment in early diabetes. Our results provide evidence that L-arginine and SOD mimics have potential in preventing and treating metabolic disturbances accompanying this widespread metabolic disease.",
journal = "Chemico-Biological Interactions",
title = "Early energy metabolism-related molecular events in skeletal muscle of diabetic rats: The effects of l -arginine and SOD mimic",
volume = "272",
doi = "10.1016/j.cbi.2017.05.003",
pages = "188-196"
}

Stančić, A., Filipović, M., Ivanović-Burmazović, I., Mašović, S., Janković, A., Otašević, V., Korać, A., Buzadžić, B.,& Korać, B.. (2017). Early energy metabolism-related molecular events in skeletal muscle of diabetic rats: The effects of l -arginine and SOD mimic. in Chemico-Biological Interactions, 272, 188-196.
https://doi.org/10.1016/j.cbi.2017.05.003

Stančić A, Filipović M, Ivanović-Burmazović I, Mašović S, Janković A, Otašević V, Korać A, Buzadžić B, Korać B. Early energy metabolism-related molecular events in skeletal muscle of diabetic rats: The effects of l -arginine and SOD mimic. in Chemico-Biological Interactions. 2017;272:188-196.
doi:10.1016/j.cbi.2017.05.003 .

Stančić, Ana, Filipović, Miloš, Ivanović-Burmazović, Ivana, Mašović, Sava, Janković, Aleksandra, Otašević, Vesna, Korać, Aleksandra, Buzadžić, Biljana, Korać, Bato, "Early energy metabolism-related molecular events in skeletal muscle of diabetic rats: The effects of l -arginine and SOD mimic" in Chemico-Biological Interactions, 272 (2017):188-196,
https://doi.org/10.1016/j.cbi.2017.05.003 . .

TY  - JOUR
AU  - Janković, Aleksandra
AU  - Otašević, Vesna
AU  - Stančić, Ana
AU  - Buzadžić, Biljana
AU  - Korać, Aleksandra
AU  - Korać, Bato
PY  - 2017
UR  - http://www.degruyter.com/view/j/hmbci.2017.31.issue-1/hmbci-2017-0034/hmbci-2017-0034.xml
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2877
AB  - Great progress has been made in our understanding of the browning process in white adipose tissue (WAT) in rodents. The recognition that i) adult humans have physiologically inducible brown adipose tissue (BAT) that may facilitate resistance to obesity and ii) that adult human BAT molecularly and functionally resembles beige adipose tissue in rodents, reignited optimism that obesity and obesity-related diabetes type 2 can be battled by controlling the browning of WAT. In this review the main cellular mechanisms and molecular mediators of browning of WAT in different physiological states are summarized. The relevance of browning of WAT in metabolic health is considered primarily through a modulation of biological role of fat tissue in overall metabolic homeostasis.
T2  - Hormone Molecular Biology and Clinical Investigation
T1  - Physiological regulation and metabolic role of browning in white adipose tissue
IS  - 1
VL  - 31
DO  - 10.1515/hmbci-2017-0034
SP  - 20170034
EP  - 20170034
ER  - 

@article{
author = "Janković, Aleksandra and Otašević, Vesna and Stančić, Ana and Buzadžić, Biljana and Korać, Aleksandra and Korać, Bato",
year = "2017",
abstract = "Great progress has been made in our understanding of the browning process in white adipose tissue (WAT) in rodents. The recognition that i) adult humans have physiologically inducible brown adipose tissue (BAT) that may facilitate resistance to obesity and ii) that adult human BAT molecularly and functionally resembles beige adipose tissue in rodents, reignited optimism that obesity and obesity-related diabetes type 2 can be battled by controlling the browning of WAT. In this review the main cellular mechanisms and molecular mediators of browning of WAT in different physiological states are summarized. The relevance of browning of WAT in metabolic health is considered primarily through a modulation of biological role of fat tissue in overall metabolic homeostasis.",
journal = "Hormone Molecular Biology and Clinical Investigation",
title = "Physiological regulation and metabolic role of browning in white adipose tissue",
number = "1",
volume = "31",
doi = "10.1515/hmbci-2017-0034",
pages = "20170034-20170034"
}

Janković, A., Otašević, V., Stančić, A., Buzadžić, B., Korać, A.,& Korać, B.. (2017). Physiological regulation and metabolic role of browning in white adipose tissue. in Hormone Molecular Biology and Clinical Investigation, 31(1), 20170034-20170034.
https://doi.org/10.1515/hmbci-2017-0034

Janković A, Otašević V, Stančić A, Buzadžić B, Korać A, Korać B. Physiological regulation and metabolic role of browning in white adipose tissue. in Hormone Molecular Biology and Clinical Investigation. 2017;31(1):20170034-20170034.
doi:10.1515/hmbci-2017-0034 .

Janković, Aleksandra, Otašević, Vesna, Stančić, Ana, Buzadžić, Biljana, Korać, Aleksandra, Korać, Bato, "Physiological regulation and metabolic role of browning in white adipose tissue" in Hormone Molecular Biology and Clinical Investigation, 31, no. 1 (2017):20170034-20170034,
https://doi.org/10.1515/hmbci-2017-0034 . .

TY  - JOUR
AU  - Janković, Aleksandra
AU  - Ferreri, Carla
AU  - Filipović, Miloš
AU  - Ivanović-Burmazović, Ivana
AU  - Stančić, Ana
AU  - Otašević, Vesna
AU  - Korać, Aleksandra
AU  - Buzadžić, Biljana
AU  - Korać, Bato
PY  - 2016
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6211
AB  - Setting the correct ratio of superoxide anion (O2•-) and nitric oxide (•NO) radicals seems to be crucial in restoring disrupted redox signaling in diabetic skin and improvement of •NO physiological action for prevention and treatment of skin injuries in diabetes. In this study we examined the effects of L-arginine and manganese(II)-pentaazamacrocyclic superoxide dismutase (SOD) mimic - M40403 in diabetic rat skin. Following induction of diabetes by alloxan (blood glucose level ≥12 mMol l -1) non-diabetic and diabetic male Mill Hill hybrid hooded rats were divided into three subgroups: (i) control, and receiving: (ii) L-arginine, (iii) M40403. Treatment of diabetic animals started after diabetes induction and lasted for 7 days. Compared to control, lower cutaneous immuno-expression of endothelial NO synthase (eNOS), heme oxygenase 1 (HO1), manganese SOD (MnSOD) and glutathione peroxidase (GSH-Px), in parallel with increased NFE2-related factor 2 (Nrf2) and nitrotyrosine levels characterized diabetic skin. L-arginine and M40403 treatments normalized alloxan-induced increase in nitrotyrosine. This was accompanied by the improvement/restitution of eNOS and HO1 or MnSOD and GSH-Px protein expression levels in diabetic skin following L-arginine, i.e. SOD mimic treatments, respectively. The results indicate that L-arginine and M40403 stabilize redox balance in diabetic skin and suggest the underlying molecular mechanisms. Restitution of skin redox balance by L-arginine and M40403 may represent an effective strategy to ameliorate therapy of diabetic skin.
PB  - Taylor & Francis
T2  - Free Radical Research
T1  - Targeting the superoxide/nitric oxide ratio by L arginine and SOD mimic in rat diabetic skin
IS  - Sup1
VL  - 50
DO  - 10.1080/10715762.2016.1232483
SP  - S51
EP  - S63
ER  - 

@article{
author = "Janković, Aleksandra and Ferreri, Carla and Filipović, Miloš and Ivanović-Burmazović, Ivana and Stančić, Ana and Otašević, Vesna and Korać, Aleksandra and Buzadžić, Biljana and Korać, Bato",
year = "2016",
abstract = "Setting the correct ratio of superoxide anion (O2•-) and nitric oxide (•NO) radicals seems to be crucial in restoring disrupted redox signaling in diabetic skin and improvement of •NO physiological action for prevention and treatment of skin injuries in diabetes. In this study we examined the effects of L-arginine and manganese(II)-pentaazamacrocyclic superoxide dismutase (SOD) mimic - M40403 in diabetic rat skin. Following induction of diabetes by alloxan (blood glucose level ≥12 mMol l -1) non-diabetic and diabetic male Mill Hill hybrid hooded rats were divided into three subgroups: (i) control, and receiving: (ii) L-arginine, (iii) M40403. Treatment of diabetic animals started after diabetes induction and lasted for 7 days. Compared to control, lower cutaneous immuno-expression of endothelial NO synthase (eNOS), heme oxygenase 1 (HO1), manganese SOD (MnSOD) and glutathione peroxidase (GSH-Px), in parallel with increased NFE2-related factor 2 (Nrf2) and nitrotyrosine levels characterized diabetic skin. L-arginine and M40403 treatments normalized alloxan-induced increase in nitrotyrosine. This was accompanied by the improvement/restitution of eNOS and HO1 or MnSOD and GSH-Px protein expression levels in diabetic skin following L-arginine, i.e. SOD mimic treatments, respectively. The results indicate that L-arginine and M40403 stabilize redox balance in diabetic skin and suggest the underlying molecular mechanisms. Restitution of skin redox balance by L-arginine and M40403 may represent an effective strategy to ameliorate therapy of diabetic skin.",
publisher = "Taylor & Francis",
journal = "Free Radical Research",
title = "Targeting the superoxide/nitric oxide ratio by L arginine and SOD mimic in rat diabetic skin",
number = "Sup1",
volume = "50",
doi = "10.1080/10715762.2016.1232483",
pages = "S51-S63"
}

Janković, A., Ferreri, C., Filipović, M., Ivanović-Burmazović, I., Stančić, A., Otašević, V., Korać, A., Buzadžić, B.,& Korać, B.. (2016). Targeting the superoxide/nitric oxide ratio by L arginine and SOD mimic in rat diabetic skin. in Free Radical Research
Taylor & Francis., 50(Sup1), S51-S63.
https://doi.org/10.1080/10715762.2016.1232483

Janković A, Ferreri C, Filipović M, Ivanović-Burmazović I, Stančić A, Otašević V, Korać A, Buzadžić B, Korać B. Targeting the superoxide/nitric oxide ratio by L arginine and SOD mimic in rat diabetic skin. in Free Radical Research. 2016;50(Sup1):S51-S63.
doi:10.1080/10715762.2016.1232483 .

Janković, Aleksandra, Ferreri, Carla, Filipović, Miloš, Ivanović-Burmazović, Ivana, Stančić, Ana, Otašević, Vesna, Korać, Aleksandra, Buzadžić, Biljana, Korać, Bato, "Targeting the superoxide/nitric oxide ratio by L arginine and SOD mimic in rat diabetic skin" in Free Radical Research, 50, no. Sup1 (2016):S51-S63,
https://doi.org/10.1080/10715762.2016.1232483 . .

TY  - JOUR
AU  - Otašević, Vesna
AU  - Šurlan, Lela
AU  - Vučetić, Milica
AU  - Tulić, Ivan
AU  - Buzadžić, Biljana
AU  - Stančić, Ana
AU  - Janković, Aleksandra
AU  - Veličković, Ksenija
AU  - Golić, Igor
AU  - Markelić, Milica
AU  - Korać, Aleksandra
AU  - Korać, Bato
PY  - 2016
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6213
AB  - Developmental dysfunction in embryos, such as a lethal level of fragmentation, is assumed to be mitochondrial in origin. This study investigated the molecular basis of mitochondrial impairment in embryo fragmentation. Transcription patterns of factors that determine mitochondrial functionality: (i) components of the oxidative phosphorylation (OXPHOS) - complex I, cytochrome b, complex IV and ATP synthase; (ii) mitochondrial membrane potential (MMP); (iii) mitochondrial DNA (mtDNA) content and (iv) proteins involved in mitochondrial dynamics, mitofusin 1 (Mfn1) and dynamin related protein 1 (Drp1) were examined in six-cells Day 3 non-fragmented (control), low-fragmented (LF) and high-fragmented (HF) human embryos. Gene expression of mitochondria-encoded components of complex I and IV, cytochrome b and mtDNA were increased in HF embryos compared with control and LF embryos. In LF embryos, expression of these molecules was decreased compared with control and HF embryos. Both classes of fragmented embryos had decreased MMP compared with control. LF embryos had increased gene expression of Mfn1 accompanied by decreased expression of Drp1, while HF embryos had decreased Mfn1 expression but increased Drp1 expression. The study revealed that each improper transcriptional (in)activation of mitochondria-encoded components of the OXPHOS during early in vitro embryo development is associated with a decrease in MMP and with embryo fragmentation. The results also showed the importance of mitochondrial dynamics in fragmentation, at least in the extent of this process.
PB  - CSIRO Publishing
T2  - Reproduction, Fertility and Development
T1  - Expression patterns of mitochondrial OXPHOS components, mitofusin 1 and dynamin-related protein 1 are associated with human embryo fragmentation
IS  - 3
VL  - 28
DO  - 10.1071/RD13415
SP  - 319
EP  - 327
ER  - 

@article{
author = "Otašević, Vesna and Šurlan, Lela and Vučetić, Milica and Tulić, Ivan and Buzadžić, Biljana and Stančić, Ana and Janković, Aleksandra and Veličković, Ksenija and Golić, Igor and Markelić, Milica and Korać, Aleksandra and Korać, Bato",
year = "2016",
abstract = "Developmental dysfunction in embryos, such as a lethal level of fragmentation, is assumed to be mitochondrial in origin. This study investigated the molecular basis of mitochondrial impairment in embryo fragmentation. Transcription patterns of factors that determine mitochondrial functionality: (i) components of the oxidative phosphorylation (OXPHOS) - complex I, cytochrome b, complex IV and ATP synthase; (ii) mitochondrial membrane potential (MMP); (iii) mitochondrial DNA (mtDNA) content and (iv) proteins involved in mitochondrial dynamics, mitofusin 1 (Mfn1) and dynamin related protein 1 (Drp1) were examined in six-cells Day 3 non-fragmented (control), low-fragmented (LF) and high-fragmented (HF) human embryos. Gene expression of mitochondria-encoded components of complex I and IV, cytochrome b and mtDNA were increased in HF embryos compared with control and LF embryos. In LF embryos, expression of these molecules was decreased compared with control and HF embryos. Both classes of fragmented embryos had decreased MMP compared with control. LF embryos had increased gene expression of Mfn1 accompanied by decreased expression of Drp1, while HF embryos had decreased Mfn1 expression but increased Drp1 expression. The study revealed that each improper transcriptional (in)activation of mitochondria-encoded components of the OXPHOS during early in vitro embryo development is associated with a decrease in MMP and with embryo fragmentation. The results also showed the importance of mitochondrial dynamics in fragmentation, at least in the extent of this process.",
publisher = "CSIRO Publishing",
journal = "Reproduction, Fertility and Development",
title = "Expression patterns of mitochondrial OXPHOS components, mitofusin 1 and dynamin-related protein 1 are associated with human embryo fragmentation",
number = "3",
volume = "28",
doi = "10.1071/RD13415",
pages = "319-327"
}

Otašević, V., Šurlan, L., Vučetić, M., Tulić, I., Buzadžić, B., Stančić, A., Janković, A., Veličković, K., Golić, I., Markelić, M., Korać, A.,& Korać, B.. (2016). Expression patterns of mitochondrial OXPHOS components, mitofusin 1 and dynamin-related protein 1 are associated with human embryo fragmentation. in Reproduction, Fertility and Development
CSIRO Publishing., 28(3), 319-327.
https://doi.org/10.1071/RD13415

Otašević V, Šurlan L, Vučetić M, Tulić I, Buzadžić B, Stančić A, Janković A, Veličković K, Golić I, Markelić M, Korać A, Korać B. Expression patterns of mitochondrial OXPHOS components, mitofusin 1 and dynamin-related protein 1 are associated with human embryo fragmentation. in Reproduction, Fertility and Development. 2016;28(3):319-327.
doi:10.1071/RD13415 .

Otašević, Vesna, Šurlan, Lela, Vučetić, Milica, Tulić, Ivan, Buzadžić, Biljana, Stančić, Ana, Janković, Aleksandra, Veličković, Ksenija, Golić, Igor, Markelić, Milica, Korać, Aleksandra, Korać, Bato, "Expression patterns of mitochondrial OXPHOS components, mitofusin 1 and dynamin-related protein 1 are associated with human embryo fragmentation" in Reproduction, Fertility and Development, 28, no. 3 (2016):319-327,
https://doi.org/10.1071/RD13415 . .