Activation of AMPK/SIRT1 axis is required for adiponectin-mediated preconditioning on myocardial ischemia-reperfusion (I/R) injury in rats
Adiponectin (AD) cardioprotective activities are mediated by AMPK, a fuel-sensing molecule sharing common targets and cellular activities with SIRT-1. Whether AD preconditioning may involve SIRT-1 activity is not known; however, the protective role of SIRT-1 during ischemia and the potential interpl...
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| Published in | PloS one Vol. 14; no. 1; p. e0210654 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
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United States
Public Library of Science
01.01.2019
Public Library of Science (PLoS) |
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| Abstract | Adiponectin (AD) cardioprotective activities are mediated by AMPK, a fuel-sensing molecule sharing common targets and cellular activities with SIRT-1. Whether AD preconditioning may involve SIRT-1 activity is not known; however, the protective role of SIRT-1 during ischemia and the potential interplay between AMPK and SIRT-1 suggest this possibility.
Isolated hearts from male Sprague-Dawley rats (n = 85) underwent ischemia/reperfusion (I/R, 30/180 min). Preconditioning with resveratrol (RSV, SIRT-1 activator) was compared to preconditioning with AD alone, or in combination with compound C (CC, AMPK inhibitor) or sirtinol (STN, SIRT-1 inhibitor). For each heart, left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (dLVP), coronary flow (CF) and left ventricular infarct mass (IM) were measured, together with the phosphorylation/activation status of AMPK, LKB1, eNOS and SIRT-1, at the beginning (15 min) and at the end (180 min) of reperfusion.
When compared to I/R, both RSV and AD improved cardiac function and reduced IM (p < 0.01, p < 0.05, respectively). Cardioprotective effects of AD were completely reversed in the AD+CC group, and significantly attenuated in the AD+STN group. Both RSV and AD increased eNOS, AMPK and LKB1 phosphorylation (for each parameter: p < 0.05 vs. I/R, in both RSV and AD treatment groups) at 15 min of reperfusion, and SIRT-1 activity at the end of reperfusion (p < 0.01, p < 0.05 vs. I/R, respectively). Interestingly, AD-mediated phosphorylation of AMPK and LKB1, and SIRT-1 deacetylation activity was markedly reduced in both the AD+CC and AD+STN groups (p < 0.05 vs. AD). Thus, AD-mediated cardioprotection requires both AMPK and SIRT-1 signaling pathways, that act as a component of a cycle and regulate each other's activities. |
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| AbstractList | Adiponectin (AD) cardioprotective activities are mediated by AMPK, a fuel-sensing molecule sharing common targets and cellular activities with SIRT-1. Whether AD preconditioning may involve SIRT-1 activity is not known; however, the protective role of SIRT-1 during ischemia and the potential interplay between AMPK and SIRT-1 suggest this possibility.
Isolated hearts from male Sprague-Dawley rats (n = 85) underwent ischemia/reperfusion (I/R, 30/180 min). Preconditioning with resveratrol (RSV, SIRT-1 activator) was compared to preconditioning with AD alone, or in combination with compound C (CC, AMPK inhibitor) or sirtinol (STN, SIRT-1 inhibitor). For each heart, left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (dLVP), coronary flow (CF) and left ventricular infarct mass (IM) were measured, together with the phosphorylation/activation status of AMPK, LKB1, eNOS and SIRT-1, at the beginning (15 min) and at the end (180 min) of reperfusion.
When compared to I/R, both RSV and AD improved cardiac function and reduced IM (p < 0.01, p < 0.05, respectively). Cardioprotective effects of AD were completely reversed in the AD+CC group, and significantly attenuated in the AD+STN group. Both RSV and AD increased eNOS, AMPK and LKB1 phosphorylation (for each parameter: p < 0.05 vs. I/R, in both RSV and AD treatment groups) at 15 min of reperfusion, and SIRT-1 activity at the end of reperfusion (p < 0.01, p < 0.05 vs. I/R, respectively). Interestingly, AD-mediated phosphorylation of AMPK and LKB1, and SIRT-1 deacetylation activity was markedly reduced in both the AD+CC and AD+STN groups (p < 0.05 vs. AD). Thus, AD-mediated cardioprotection requires both AMPK and SIRT-1 signaling pathways, that act as a component of a cycle and regulate each other's activities. Background Adiponectin (AD) cardioprotective activities are mediated by AMPK, a fuel-sensing molecule sharing common targets and cellular activities with SIRT-1. Whether AD preconditioning may involve SIRT-1 activity is not known; however, the protective role of SIRT-1 during ischemia and the potential interplay between AMPK and SIRT-1 suggest this possibility. Methods Isolated hearts from male Sprague-Dawley rats (n = 85) underwent ischemia/reperfusion (I/R, 30/180 min). Preconditioning with resveratrol (RSV, SIRT-1 activator) was compared to preconditioning with AD alone, or in combination with compound C (CC, AMPK inhibitor) or sirtinol (STN, SIRT-1 inhibitor). For each heart, left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (dLVP), coronary flow (CF) and left ventricular infarct mass (IM) were measured, together with the phosphorylation/activation status of AMPK, LKB1, eNOS and SIRT-1, at the beginning (15 min) and at the end (180 min) of reperfusion. Results and conclusions When compared to I/R, both RSV and AD improved cardiac function and reduced IM (p < 0.01, p < 0.05, respectively). Cardioprotective effects of AD were completely reversed in the AD+CC group, and significantly attenuated in the AD+STN group. Both RSV and AD increased eNOS, AMPK and LKB1 phosphorylation (for each parameter: p < 0.05 vs. I/R, in both RSV and AD treatment groups) at 15 min of reperfusion, and SIRT-1 activity at the end of reperfusion (p < 0.01, p < 0.05 vs. I/R, respectively). Interestingly, AD-mediated phosphorylation of AMPK and LKB1, and SIRT-1 deacetylation activity was markedly reduced in both the AD+CC and AD+STN groups (p < 0.05 vs. AD). Thus, AD-mediated cardioprotection requires both AMPK and SIRT-1 signaling pathways, that act as a component of a cycle and regulate each other’s activities. Background Adiponectin (AD) cardioprotective activities are mediated by AMPK, a fuel-sensing molecule sharing common targets and cellular activities with SIRT-1. Whether AD preconditioning may involve SIRT-1 activity is not known; however, the protective role of SIRT-1 during ischemia and the potential interplay between AMPK and SIRT-1 suggest this possibility. Methods Isolated hearts from male Sprague-Dawley rats (n = 85) underwent ischemia/reperfusion (I/R, 30/180 min). Preconditioning with resveratrol (RSV, SIRT-1 activator) was compared to preconditioning with AD alone, or in combination with compound C (CC, AMPK inhibitor) or sirtinol (STN, SIRT-1 inhibitor). For each heart, left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (dLVP), coronary flow (CF) and left ventricular infarct mass (IM) were measured, together with the phosphorylation/activation status of AMPK, LKB1, eNOS and SIRT-1, at the beginning (15 min) and at the end (180 min) of reperfusion. Results and conclusions When compared to I/R, both RSV and AD improved cardiac function and reduced IM (p < 0.01, p < 0.05, respectively). Cardioprotective effects of AD were completely reversed in the AD+CC group, and significantly attenuated in the AD+STN group. Both RSV and AD increased eNOS, AMPK and LKB1 phosphorylation (for each parameter: p < 0.05 vs. I/R, in both RSV and AD treatment groups) at 15 min of reperfusion, and SIRT-1 activity at the end of reperfusion (p < 0.01, p < 0.05 vs. I/R, respectively). Interestingly, AD-mediated phosphorylation of AMPK and LKB1, and SIRT-1 deacetylation activity was markedly reduced in both the AD+CC and AD+STN groups (p < 0.05 vs. AD). Thus, AD-mediated cardioprotection requires both AMPK and SIRT-1 signaling pathways, that act as a component of a cycle and regulate each other's activities. BackgroundAdiponectin (AD) cardioprotective activities are mediated by AMPK, a fuel-sensing molecule sharing common targets and cellular activities with SIRT-1. Whether AD preconditioning may involve SIRT-1 activity is not known; however, the protective role of SIRT-1 during ischemia and the potential interplay between AMPK and SIRT-1 suggest this possibility.MethodsIsolated hearts from male Sprague-Dawley rats (n = 85) underwent ischemia/reperfusion (I/R, 30/180 min). Preconditioning with resveratrol (RSV, SIRT-1 activator) was compared to preconditioning with AD alone, or in combination with compound C (CC, AMPK inhibitor) or sirtinol (STN, SIRT-1 inhibitor). For each heart, left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (dLVP), coronary flow (CF) and left ventricular infarct mass (IM) were measured, together with the phosphorylation/activation status of AMPK, LKB1, eNOS and SIRT-1, at the beginning (15 min) and at the end (180 min) of reperfusion.Results and conclusionsWhen compared to I/R, both RSV and AD improved cardiac function and reduced IM (p < 0.01, p < 0.05, respectively). Cardioprotective effects of AD were completely reversed in the AD+CC group, and significantly attenuated in the AD+STN group. Both RSV and AD increased eNOS, AMPK and LKB1 phosphorylation (for each parameter: p < 0.05 vs. I/R, in both RSV and AD treatment groups) at 15 min of reperfusion, and SIRT-1 activity at the end of reperfusion (p < 0.01, p < 0.05 vs. I/R, respectively). Interestingly, AD-mediated phosphorylation of AMPK and LKB1, and SIRT-1 deacetylation activity was markedly reduced in both the AD+CC and AD+STN groups (p < 0.05 vs. AD). Thus, AD-mediated cardioprotection requires both AMPK and SIRT-1 signaling pathways, that act as a component of a cycle and regulate each other's activities. Adiponectin (AD) cardioprotective activities are mediated by AMPK, a fuel-sensing molecule sharing common targets and cellular activities with SIRT-1. Whether AD preconditioning may involve SIRT-1 activity is not known; however, the protective role of SIRT-1 during ischemia and the potential interplay between AMPK and SIRT-1 suggest this possibility. Isolated hearts from male Sprague-Dawley rats (n = 85) underwent ischemia/reperfusion (I/R, 30/180 min). Preconditioning with resveratrol (RSV, SIRT-1 activator) was compared to preconditioning with AD alone, or in combination with compound C (CC, AMPK inhibitor) or sirtinol (STN, SIRT-1 inhibitor). For each heart, left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (dLVP), coronary flow (CF) and left ventricular infarct mass (IM) were measured, together with the phosphorylation/activation status of AMPK, LKB1, eNOS and SIRT-1, at the beginning (15 min) and at the end (180 min) of reperfusion. When compared to I/R, both RSV and AD improved cardiac function and reduced IM (p < 0.01, p < 0.05, respectively). Cardioprotective effects of AD were completely reversed in the AD+CC group, and significantly attenuated in the AD+STN group. Both RSV and AD increased eNOS, AMPK and LKB1 phosphorylation (for each parameter: p < 0.05 vs. I/R, in both RSV and AD treatment groups) at 15 min of reperfusion, and SIRT-1 activity at the end of reperfusion (p < 0.01, p < 0.05 vs. I/R, respectively). Interestingly, AD-mediated phosphorylation of AMPK and LKB1, and SIRT-1 deacetylation activity was markedly reduced in both the AD+CC and AD+STN groups (p < 0.05 vs. AD). Thus, AD-mediated cardioprotection requires both AMPK and SIRT-1 signaling pathways, that act as a component of a cycle and regulate each other's activities. |
| Audience | Academic |
| Author | Nacci, Carmela Leo, Valentina De Salvia, Maria Antonietta Montagnani, Monica Potenza, Maria Assunta Sgarra, Luca |
| AuthorAffiliation | Indiana University School of Medicine, UNITED STATES 1 Department of Biomedical Sciences and Human Oncology-Pharmacology Section, Medical School-University of Bari "Aldo Moro", Bari, Italy 2 Department of Emergency and Organ Transplantation-Section of Cardiovascular Diseases, Medical School-University of Bari "Aldo Moro", Bari, Italy |
| AuthorAffiliation_xml | – name: Indiana University School of Medicine, UNITED STATES – name: 1 Department of Biomedical Sciences and Human Oncology-Pharmacology Section, Medical School-University of Bari "Aldo Moro", Bari, Italy – name: 2 Department of Emergency and Organ Transplantation-Section of Cardiovascular Diseases, Medical School-University of Bari "Aldo Moro", Bari, Italy |
| Author_xml | – sequence: 1 givenname: Maria Assunta surname: Potenza fullname: Potenza, Maria Assunta organization: Department of Biomedical Sciences and Human Oncology-Pharmacology Section, Medical School-University of Bari "Aldo Moro", Bari, Italy – sequence: 2 givenname: Luca surname: Sgarra fullname: Sgarra, Luca organization: Department of Emergency and Organ Transplantation-Section of Cardiovascular Diseases, Medical School-University of Bari "Aldo Moro", Bari, Italy – sequence: 3 givenname: Carmela surname: Nacci fullname: Nacci, Carmela organization: Department of Biomedical Sciences and Human Oncology-Pharmacology Section, Medical School-University of Bari "Aldo Moro", Bari, Italy – sequence: 4 givenname: Valentina surname: Leo fullname: Leo, Valentina organization: Department of Biomedical Sciences and Human Oncology-Pharmacology Section, Medical School-University of Bari "Aldo Moro", Bari, Italy – sequence: 5 givenname: Maria Antonietta orcidid: 0000-0001-5326-792X surname: De Salvia fullname: De Salvia, Maria Antonietta organization: Department of Biomedical Sciences and Human Oncology-Pharmacology Section, Medical School-University of Bari "Aldo Moro", Bari, Italy – sequence: 6 givenname: Monica orcidid: 0000-0002-5697-8185 surname: Montagnani fullname: Montagnani, Monica organization: Department of Biomedical Sciences and Human Oncology-Pharmacology Section, Medical School-University of Bari "Aldo Moro", Bari, Italy |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30653603$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | COPYRIGHT 2019 Public Library of Science 2019 Potenza et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2019 Potenza et al 2019 Potenza et al |
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| DocumentTitleAlternate | SIRT1 participates to adiponectin-mediated cardiac protection during preconditioning |
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| References | D Kukidome (ref15) 2006; 55 S Imai (ref7) 2000; 403 S Nemoto (ref22) 2004; 306 S Winnik (ref13) 2012; 10 J Galvao (ref44) 2014; 28 Y Liu (ref48) 1996; 78 P Ferdinandy (ref3) 2014; 66 M Sulaiman (ref53) 2009; 298 F Addabbo (ref35) 2011; 301 D Qi (ref6) 2015; 26 C Canto (ref8) 2009; 20 A Skyschally (ref50) 2015; 117 M Fulco (ref61) 2008; 14 T Pischon (ref33) 2004; 291 G Heusch (ref20) 2000; 87 X Hou (ref63) 2008; 283 M Debinski (ref40) 2011; 27 S Lecour (ref49) 2005; 112 GM Rosano (ref4) 2008; 14 RR Russell 3rd (ref16) 2004; 114 JW Calvert (ref56) 2008; 57 DJ Hausenloy (ref2) 2016; 13 S Kojima (ref64) 2003; 89 D Chen (ref21) 2008; 22 CP Hsu (ref27) 2010; 122 K Ohashi (ref32) 2006; 47 L Sgarra (ref42) 2014; 9 Y Hattori (ref37) 2003; 46 K Carvajal (ref17) 2007; 292 N Ouchi (ref34) 2007; 380 RR Alcendor (ref26) 2007; 100 N Suleman (ref51) 2008; 79 A Hostrup (ref46) 2012; 30 A Cattelan (ref59) 2015; 70 F Lan (ref24) 2008; 283 Y Wang (ref57) 2009; 119 SM Nadtochiy (ref28) 2010; 89 P Jungtrakoon (ref45) 2011; 6 ref1 AY Chan (ref58) 2004; 279 AT Gonon (ref39) 2008; 78 J Li (ref14) 2017; 2017 H Chen (ref36) 2003; 278 LH Young (ref62) 2005; 15 G Nanayakkara (ref38) 2012; 2 SM Nadtochiy (ref29) 2011; 301 T Nystrom (ref65) 2006; 110 M Suwa (ref23) 2008; 57 R Shibata (ref41) 2005; 11 R Ferrari (ref5) 1995; 76 HY Cohen (ref11) 2004; 305 MM Bradford (ref47) 1976; 72 XS Gu (ref54) 2014; 13 JM Cotton (ref19) 2002; 88 L Wang (ref30) 2018 RR Alcendor (ref25) 2004; 95 ZP Chen (ref18) 1999; 443 D Aksentijevic (ref43) 2015; 101 LW Finley (ref9) 2009; 8 M Kumada (ref31) 2003; 23 HS Kwon (ref10) 2008; 33 C Canto (ref12) 2009; 458 L Li (ref55) 2007; 139 M Thirunavukkarasu (ref52) 2007; 43 T Sasaki (ref60) 2008; 3 |
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| Snippet | Adiponectin (AD) cardioprotective activities are mediated by AMPK, a fuel-sensing molecule sharing common targets and cellular activities with SIRT-1. Whether... Background Adiponectin (AD) cardioprotective activities are mediated by AMPK, a fuel-sensing molecule sharing common targets and cellular activities with... BACKGROUNDAdiponectin (AD) cardioprotective activities are mediated by AMPK, a fuel-sensing molecule sharing common targets and cellular activities with... BackgroundAdiponectin (AD) cardioprotective activities are mediated by AMPK, a fuel-sensing molecule sharing common targets and cellular activities with... Background Adiponectin (AD) cardioprotective activities are mediated by AMPK, a fuel-sensing molecule sharing common targets and cellular activities with... |
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| SubjectTerms | Activation Adiponectin Adiponectin - genetics Adiponectin - metabolism AMP-Activated Protein Kinases - metabolism Animals Apoptosis Biology and Life Sciences Blood pressure Cardiac function Cardiomyocytes Cardiotonic agents Cardiovascular disease Deacetylation Diabetes Diastolic pressure Heart Heart attacks Hypertension Inhibitors Ischemia Ischemic Preconditioning - methods Kinases Laboratory animals LKB1 protein Male Medical prognosis Medical schools Medicine and Health Sciences Metabolism Myocardial ischemia Myocardial Reperfusion Injury - metabolism Nitric oxide Oncology Pharmacology Phosphorylation Physiological aspects Preconditioning Protein hormones Proteins Rats Rats, Sprague-Dawley Reperfusion Reperfusion injury Research and Analysis Methods Resveratrol Rodents Signal Transduction - physiology SIRT1 protein Sirtuin 1 - metabolism Tumor necrosis factor-TNF Ventricle |
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| Title | Activation of AMPK/SIRT1 axis is required for adiponectin-mediated preconditioning on myocardial ischemia-reperfusion (I/R) injury in rats |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/30653603 https://www.proquest.com/docview/2168182545 https://search.proquest.com/docview/2179406087 https://pubmed.ncbi.nlm.nih.gov/PMC6336234 https://doaj.org/article/fb425fdd9d05489a805239cb84c89881 http://dx.doi.org/10.1371/journal.pone.0210654 |
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