TY  - JOUR
AU  - Živanović, Jasmina
AU  - Kouroussis, Emilia
AU  - Kohl, Joshua B.
AU  - Adhikari, Bikash
AU  - Bursać, Biljana
AU  - Schott-Roux, Sonia
AU  - Petrović, Dunja
AU  - Miljković, Jan Lj.
AU  - Thomas-Lopez, Daniel
AU  - Jung, Youngeun
AU  - Miler, Marko
AU  - Mitchell, Sarah
AU  - Milošević, Verica
AU  - Gomes, Jose Eduardo
AU  - Benhar, Moran
AU  - Gonzales-Zorn, Bruno
AU  - Ivanović-Burmazović, Ivana
AU  - Torregrossa, Roberta
AU  - Mitchell, James R.
AU  - Whiteman, Matthew
AU  - Schwarz, Guenter
AU  - Snyder, Solomon H.
AU  - Paul, Bindu D.
AU  - Carroll, Kate S.
AU  - Filipović, Miloš R.
PY  - 2019
UR  - https://www.sciencedirect.com/science/article/abs/pii/S1550413119305625
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3518
AB  - Life on Earth emerged in a hydrogen sulfide (H2S)-rich environment eons ago and with it protein persulfidation mediated by H2S evolved as a signaling mechanism. Protein persulfidation (S-sulfhydration) is a post-translational modification of reactive cysteine residues, which modulate protein structure and/or function. Persulfides are difficult to label and study due to their reactivity and similarity with cysteine. Here, we report a facile strategy for chemoselective persulfide bioconjugation using dimedone-based probes, to achieve highly selective, rapid, and robust persulfide labeling in biological samples with broad utility. Using this method, we show persulfidation is an evolutionarily conserved modification and waves of persulfidation are employed by cells to resolve sulfenylation and prevent irreversible cysteine overoxidation preserving protein function. We report an age-associated decline in persulfidation that is conserved across evolutionary boundaries. Accordingly, dietary or pharmacological interventions to increase persulfidation associate with increased longevity and improved capacity to cope with stress stimuli.
T2  - Cell Metabolism
T1  - Selective Persulfide Detection Reveals Evolutionarily Conserved Antiaging Effects of S-Sulfhydration
IS  - 6
VL  - 30
DO  - 10.1016/J.CMET.2019.10.007
SP  - 1152
EP  - 1170.e13
ER  - 

@article{
author = "Živanović, Jasmina and Kouroussis, Emilia and Kohl, Joshua B. and Adhikari, Bikash and Bursać, Biljana and Schott-Roux, Sonia and Petrović, Dunja and Miljković, Jan Lj. and Thomas-Lopez, Daniel and Jung, Youngeun and Miler, Marko and Mitchell, Sarah and Milošević, Verica and Gomes, Jose Eduardo and Benhar, Moran and Gonzales-Zorn, Bruno and Ivanović-Burmazović, Ivana and Torregrossa, Roberta and Mitchell, James R. and Whiteman, Matthew and Schwarz, Guenter and Snyder, Solomon H. and Paul, Bindu D. and Carroll, Kate S. and Filipović, Miloš R.",
year = "2019",
abstract = "Life on Earth emerged in a hydrogen sulfide (H2S)-rich environment eons ago and with it protein persulfidation mediated by H2S evolved as a signaling mechanism. Protein persulfidation (S-sulfhydration) is a post-translational modification of reactive cysteine residues, which modulate protein structure and/or function. Persulfides are difficult to label and study due to their reactivity and similarity with cysteine. Here, we report a facile strategy for chemoselective persulfide bioconjugation using dimedone-based probes, to achieve highly selective, rapid, and robust persulfide labeling in biological samples with broad utility. Using this method, we show persulfidation is an evolutionarily conserved modification and waves of persulfidation are employed by cells to resolve sulfenylation and prevent irreversible cysteine overoxidation preserving protein function. We report an age-associated decline in persulfidation that is conserved across evolutionary boundaries. Accordingly, dietary or pharmacological interventions to increase persulfidation associate with increased longevity and improved capacity to cope with stress stimuli.",
journal = "Cell Metabolism",
title = "Selective Persulfide Detection Reveals Evolutionarily Conserved Antiaging Effects of S-Sulfhydration",
number = "6",
volume = "30",
doi = "10.1016/J.CMET.2019.10.007",
pages = "1152-1170.e13"
}

Živanović, J., Kouroussis, E., Kohl, J. B., Adhikari, B., Bursać, B., Schott-Roux, S., Petrović, D., Miljković, J. Lj., Thomas-Lopez, D., Jung, Y., Miler, M., Mitchell, S., Milošević, V., Gomes, J. E., Benhar, M., Gonzales-Zorn, B., Ivanović-Burmazović, I., Torregrossa, R., Mitchell, J. R., Whiteman, M., Schwarz, G., Snyder, S. H., Paul, B. D., Carroll, K. S.,& Filipović, M. R.. (2019). Selective Persulfide Detection Reveals Evolutionarily Conserved Antiaging Effects of S-Sulfhydration. in Cell Metabolism, 30(6), 1152-1170.e13.
https://doi.org/10.1016/J.CMET.2019.10.007

Živanović J, Kouroussis E, Kohl JB, Adhikari B, Bursać B, Schott-Roux S, Petrović D, Miljković JL, Thomas-Lopez D, Jung Y, Miler M, Mitchell S, Milošević V, Gomes JE, Benhar M, Gonzales-Zorn B, Ivanović-Burmazović I, Torregrossa R, Mitchell JR, Whiteman M, Schwarz G, Snyder SH, Paul BD, Carroll KS, Filipović MR. Selective Persulfide Detection Reveals Evolutionarily Conserved Antiaging Effects of S-Sulfhydration. in Cell Metabolism. 2019;30(6):1152-1170.e13.
doi:10.1016/J.CMET.2019.10.007 .

Živanović, Jasmina, Kouroussis, Emilia, Kohl, Joshua B., Adhikari, Bikash, Bursać, Biljana, Schott-Roux, Sonia, Petrović, Dunja, Miljković, Jan Lj., Thomas-Lopez, Daniel, Jung, Youngeun, Miler, Marko, Mitchell, Sarah, Milošević, Verica, Gomes, Jose Eduardo, Benhar, Moran, Gonzales-Zorn, Bruno, Ivanović-Burmazović, Ivana, Torregrossa, Roberta, Mitchell, James R., Whiteman, Matthew, Schwarz, Guenter, Snyder, Solomon H., Paul, Bindu D., Carroll, Kate S., Filipović, Miloš R., "Selective Persulfide Detection Reveals Evolutionarily Conserved Antiaging Effects of S-Sulfhydration" in Cell Metabolism, 30, no. 6 (2019):1152-1170.e13,
https://doi.org/10.1016/J.CMET.2019.10.007 . .

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 . .