Key role of endothelium in the eNOS-dependent cardioprotection with exercise training
Abstract Modulation of endothelial nitric oxide synthase (eNOS) activation is recognized as a main trigger of the cardioprotective effects of exercise training on heart vulnerability to ischemia-reperfusion (IR). However, this enzyme is expressed both in coronary endothelial cells and cardiomyocytes...
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| Veröffentlicht in: | Journal of molecular and cellular cardiology 2017-01, Vol.102, p.26-30 |
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| container_title | Journal of molecular and cellular cardiology |
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| creator | Farah, C Nascimento, A Bolea, G Meyer, G Gayrard, S Lacampagne, A Cazorla, O Reboul, C |
| description | Abstract Modulation of endothelial nitric oxide synthase (eNOS) activation is recognized as a main trigger of the cardioprotective effects of exercise training on heart vulnerability to ischemia-reperfusion (IR). However, this enzyme is expressed both in coronary endothelial cells and cardiomyocytes and the contribution of each one to such cardioprotection has never been challenged. The aim of this study was to investigate the role of eNOS from the cardiomyocytes vs. the endothelium in the exercise cardioprotection. Male Wistar rats were assigned to a chronic aerobic training (Ex) (vs. sedentary group; Sed) and we investigated the role of eNOS in the effects of exercise on sensitivity to IR or anoxia-reoxygenation (A/R) at whole heart, isolated cardiomyocytes and left coronary artery (LCA) levels. We observed that exercise increased eNOS activation (Ser1177 phosphorylation) and protein S-nitrosylation in whole heart but not at cardiomyocyte level, suggesting the specific target of endothelial cells by exercise. Consistently, in isolated cardiomyocytes submitted to the A/R procedure, exercise reduced cell death and improved cells contractility, but independently of the eNOS pathway. Next, to evaluate the contribution of endothelial cells in exercise cardioprotection, LCA were isolated before and after an IR procedure performed on Langendorff hearts. Exercise improved basal relaxation sensitivity to acetylcholine and markedly reduced the alteration of endothelium-dependent coronary relaxation induced by IR. Furthermore, inactivation of coronary endothelial cells activity just before IR, obtained with a bolus of Triton X-100, totally suppressed cardioprotective effects of exercise on both left ventricular functional recovery after IR and infarct size, whereas no effect of Triton X-100 was observed in Sed group. In conclusion, these results show that coronary endothelial cells rather than cardiomyocytes play a key role in the eNOS-dependent cardioprotection of exercise. |
| doi_str_mv | 10.1016/j.yjmcc.2016.11.008 |
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However, this enzyme is expressed both in coronary endothelial cells and cardiomyocytes and the contribution of each one to such cardioprotection has never been challenged. The aim of this study was to investigate the role of eNOS from the cardiomyocytes vs. the endothelium in the exercise cardioprotection. Male Wistar rats were assigned to a chronic aerobic training (Ex) (vs. sedentary group; Sed) and we investigated the role of eNOS in the effects of exercise on sensitivity to IR or anoxia-reoxygenation (A/R) at whole heart, isolated cardiomyocytes and left coronary artery (LCA) levels. We observed that exercise increased eNOS activation (Ser1177 phosphorylation) and protein S-nitrosylation in whole heart but not at cardiomyocyte level, suggesting the specific target of endothelial cells by exercise. Consistently, in isolated cardiomyocytes submitted to the A/R procedure, exercise reduced cell death and improved cells contractility, but independently of the eNOS pathway. Next, to evaluate the contribution of endothelial cells in exercise cardioprotection, LCA were isolated before and after an IR procedure performed on Langendorff hearts. Exercise improved basal relaxation sensitivity to acetylcholine and markedly reduced the alteration of endothelium-dependent coronary relaxation induced by IR. Furthermore, inactivation of coronary endothelial cells activity just before IR, obtained with a bolus of Triton X-100, totally suppressed cardioprotective effects of exercise on both left ventricular functional recovery after IR and infarct size, whereas no effect of Triton X-100 was observed in Sed group. In conclusion, these results show that coronary endothelial cells rather than cardiomyocytes play a key role in the eNOS-dependent cardioprotection of exercise.</description><identifier>ISSN: 0022-2828</identifier><identifier>EISSN: 1095-8584</identifier><identifier>DOI: 10.1016/j.yjmcc.2016.11.008</identifier><identifier>PMID: 27866931</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Animals ; Cardioprotection ; Cardiovascular ; Coronary artery ; Disease Models, Animal ; Endothelium - metabolism ; eNOS ; Exercise ; Ischemia-reperfusion ; Life Sciences ; Male ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - pathology ; Myocytes ; Myocytes, Cardiac - metabolism ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type III - metabolism ; Phosphorylation ; Physical Conditioning, Animal ; Rats ; Signal Transduction</subject><ispartof>Journal of molecular and cellular cardiology, 2017-01, Vol.102, p.26-30</ispartof><rights>2016 Elsevier Ltd</rights><rights>Copyright © 2016 Elsevier Ltd. All rights reserved.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c493t-16bd84dda5b198aa016d6b0a155d6f8939d8ed5ed82dfc453bf0c494e06c4f83</citedby><cites>FETCH-LOGICAL-c493t-16bd84dda5b198aa016d6b0a155d6f8939d8ed5ed82dfc453bf0c494e06c4f83</cites><orcidid>0000-0003-0775-203X ; 0000-0003-0264-1787</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0022282816304126$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27866931$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.umontpellier.fr/hal-01824256$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Farah, C</creatorcontrib><creatorcontrib>Nascimento, A</creatorcontrib><creatorcontrib>Bolea, G</creatorcontrib><creatorcontrib>Meyer, G</creatorcontrib><creatorcontrib>Gayrard, S</creatorcontrib><creatorcontrib>Lacampagne, A</creatorcontrib><creatorcontrib>Cazorla, O</creatorcontrib><creatorcontrib>Reboul, C</creatorcontrib><title>Key role of endothelium in the eNOS-dependent cardioprotection with exercise training</title><title>Journal of molecular and cellular cardiology</title><addtitle>J Mol Cell Cardiol</addtitle><description>Abstract Modulation of endothelial nitric oxide synthase (eNOS) activation is recognized as a main trigger of the cardioprotective effects of exercise training on heart vulnerability to ischemia-reperfusion (IR). However, this enzyme is expressed both in coronary endothelial cells and cardiomyocytes and the contribution of each one to such cardioprotection has never been challenged. The aim of this study was to investigate the role of eNOS from the cardiomyocytes vs. the endothelium in the exercise cardioprotection. Male Wistar rats were assigned to a chronic aerobic training (Ex) (vs. sedentary group; Sed) and we investigated the role of eNOS in the effects of exercise on sensitivity to IR or anoxia-reoxygenation (A/R) at whole heart, isolated cardiomyocytes and left coronary artery (LCA) levels. We observed that exercise increased eNOS activation (Ser1177 phosphorylation) and protein S-nitrosylation in whole heart but not at cardiomyocyte level, suggesting the specific target of endothelial cells by exercise. Consistently, in isolated cardiomyocytes submitted to the A/R procedure, exercise reduced cell death and improved cells contractility, but independently of the eNOS pathway. Next, to evaluate the contribution of endothelial cells in exercise cardioprotection, LCA were isolated before and after an IR procedure performed on Langendorff hearts. Exercise improved basal relaxation sensitivity to acetylcholine and markedly reduced the alteration of endothelium-dependent coronary relaxation induced by IR. Furthermore, inactivation of coronary endothelial cells activity just before IR, obtained with a bolus of Triton X-100, totally suppressed cardioprotective effects of exercise on both left ventricular functional recovery after IR and infarct size, whereas no effect of Triton X-100 was observed in Sed group. In conclusion, these results show that coronary endothelial cells rather than cardiomyocytes play a key role in the eNOS-dependent cardioprotection of exercise.</description><subject>Animals</subject><subject>Cardioprotection</subject><subject>Cardiovascular</subject><subject>Coronary artery</subject><subject>Disease Models, Animal</subject><subject>Endothelium - metabolism</subject><subject>eNOS</subject><subject>Exercise</subject><subject>Ischemia-reperfusion</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocytes</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>Phosphorylation</subject><subject>Physical Conditioning, Animal</subject><subject>Rats</subject><subject>Signal Transduction</subject><issn>0022-2828</issn><issn>1095-8584</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtv1DAURi0EotPCL0BCXsIiwW-cBUhVBS1iRBcta8uxbxiHJB7spDD_HocpXbBh5df57rWPEXpBSU0JVW_6-tCPztWsLGpKa0L0I7ShpJGVllo8RhtCGKuYZvoEnebcE0IawflTdMLeaqUaTjfo62c44BQHwLHDMPk472AIy4jDhMsUw5frm8rDvhzBNGNnkw9xn-IMbg5xwj_DvMPwC5ILGfCcbJjC9O0ZetLZIcPz-_EM3X78cHtxVW2vLz9dnG8rJxo-V1S1XgvvrWxpo60tD_GqJZZK6VWnG954DV6C18x3TkjedqQkBRDlRKf5GXp9LLuzg9mnMNp0MNEGc3W-NeseoZoJJtUdLeyrI1su_2OBPJsxZAfDYCeISzZUF1BITVaUH1GXYs4JuofalJhVvenNH_VmVW8oNUV9Sb28b7C0I_iHzF_XBXh3BKAYuQuQTHYBJgc-pGLT-Bj-0-D9P3k3FNvODt_hALmPS5qKbENNZoaYm_X318-nihNBmeK_ASzBqrc</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Farah, C</creator><creator>Nascimento, A</creator><creator>Bolea, G</creator><creator>Meyer, G</creator><creator>Gayrard, S</creator><creator>Lacampagne, A</creator><creator>Cazorla, O</creator><creator>Reboul, C</creator><general>Elsevier Ltd</general><general>Elsevier</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><orcidid>https://orcid.org/0000-0003-0775-203X</orcidid><orcidid>https://orcid.org/0000-0003-0264-1787</orcidid></search><sort><creationdate>20170101</creationdate><title>Key role of endothelium in the eNOS-dependent cardioprotection with exercise training</title><author>Farah, C ; Nascimento, A ; Bolea, G ; Meyer, G ; Gayrard, S ; Lacampagne, A ; Cazorla, O ; Reboul, C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c493t-16bd84dda5b198aa016d6b0a155d6f8939d8ed5ed82dfc453bf0c494e06c4f83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Cardioprotection</topic><topic>Cardiovascular</topic><topic>Coronary artery</topic><topic>Disease Models, Animal</topic><topic>Endothelium - metabolism</topic><topic>eNOS</topic><topic>Exercise</topic><topic>Ischemia-reperfusion</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - pathology</topic><topic>Myocytes</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type III - metabolism</topic><topic>Phosphorylation</topic><topic>Physical Conditioning, Animal</topic><topic>Rats</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Farah, C</creatorcontrib><creatorcontrib>Nascimento, A</creatorcontrib><creatorcontrib>Bolea, G</creatorcontrib><creatorcontrib>Meyer, G</creatorcontrib><creatorcontrib>Gayrard, S</creatorcontrib><creatorcontrib>Lacampagne, A</creatorcontrib><creatorcontrib>Cazorla, O</creatorcontrib><creatorcontrib>Reboul, C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><jtitle>Journal of molecular and cellular cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Farah, C</au><au>Nascimento, A</au><au>Bolea, G</au><au>Meyer, G</au><au>Gayrard, S</au><au>Lacampagne, A</au><au>Cazorla, O</au><au>Reboul, C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Key role of endothelium in the eNOS-dependent cardioprotection with exercise training</atitle><jtitle>Journal of molecular and cellular cardiology</jtitle><addtitle>J Mol Cell Cardiol</addtitle><date>2017-01-01</date><risdate>2017</risdate><volume>102</volume><spage>26</spage><epage>30</epage><pages>26-30</pages><issn>0022-2828</issn><eissn>1095-8584</eissn><abstract>Abstract Modulation of endothelial nitric oxide synthase (eNOS) activation is recognized as a main trigger of the cardioprotective effects of exercise training on heart vulnerability to ischemia-reperfusion (IR). However, this enzyme is expressed both in coronary endothelial cells and cardiomyocytes and the contribution of each one to such cardioprotection has never been challenged. The aim of this study was to investigate the role of eNOS from the cardiomyocytes vs. the endothelium in the exercise cardioprotection. Male Wistar rats were assigned to a chronic aerobic training (Ex) (vs. sedentary group; Sed) and we investigated the role of eNOS in the effects of exercise on sensitivity to IR or anoxia-reoxygenation (A/R) at whole heart, isolated cardiomyocytes and left coronary artery (LCA) levels. We observed that exercise increased eNOS activation (Ser1177 phosphorylation) and protein S-nitrosylation in whole heart but not at cardiomyocyte level, suggesting the specific target of endothelial cells by exercise. Consistently, in isolated cardiomyocytes submitted to the A/R procedure, exercise reduced cell death and improved cells contractility, but independently of the eNOS pathway. Next, to evaluate the contribution of endothelial cells in exercise cardioprotection, LCA were isolated before and after an IR procedure performed on Langendorff hearts. Exercise improved basal relaxation sensitivity to acetylcholine and markedly reduced the alteration of endothelium-dependent coronary relaxation induced by IR. Furthermore, inactivation of coronary endothelial cells activity just before IR, obtained with a bolus of Triton X-100, totally suppressed cardioprotective effects of exercise on both left ventricular functional recovery after IR and infarct size, whereas no effect of Triton X-100 was observed in Sed group. 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| subjects | Animals Cardioprotection Cardiovascular Coronary artery Disease Models, Animal Endothelium - metabolism eNOS Exercise Ischemia-reperfusion Life Sciences Male Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocytes Myocytes, Cardiac - metabolism Nitric Oxide - metabolism Nitric Oxide Synthase Type III - metabolism Phosphorylation Physical Conditioning, Animal Rats Signal Transduction |
| title | Key role of endothelium in the eNOS-dependent cardioprotection with exercise training |
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