Divergent Effects of Cyclophilin-D Inhibition on the Female Rat Heart: Acute Versus Chronic Post-Myocardial Infarction
Background/Aims: The mitochondrial permeability transition pore opening plays a critical role in the pathogenesis of myocardial infarction. Inhibition of cyclophilin-D (CyP-D), a key regulator of the mitochondrial permeability transition pore, has been shown to exert cardioprotective effects against...
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| Veröffentlicht in: | Cellular physiology and biochemistry 2018-01, Vol.50 (1), p.288-303 |
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| creator | Parodi-Rullán, Rebecca M. Soto-Prado, Jadira Vega-Lugo, Jesús Chapa-Dubocq, Xavier Díaz-Cordero, Sara I. Javadov, Sabzali |
| description | Background/Aims: The mitochondrial permeability transition pore opening plays a critical role in the pathogenesis of myocardial infarction. Inhibition of cyclophilin-D (CyP-D), a key regulator of the mitochondrial permeability transition pore, has been shown to exert cardioprotective effects against ischemia-reperfusion injury on various animal models, mostly in males. However, failure of recent clinical trials requires a detailed elucidation of the cardioprotective efficacy of CyP-D inhibition. The aim of this study was to examine whether cardioprotective effects of sanglifehrin A, a potent inhibitor of CyP-D, on post-infarcted hearts depends on reperfusion. Methods: Acute or chronic myocardial infarction was induced by coronary artery ligation with/without subsequent reperfusion for 2 and 28 days in female Sprague-Dawley rats. Cardiac function was estimated by echocardiography. Oxygen consumption rates, ROS production, permeability transition pore opening, protein carbonylation and respiratory supercomplexes were analyzed in isolated cardiac mitochondria. Results: Sanglifehrin A significantly improved cardiac function of reperfused hearts at 2 days but failed to protect after 28 days. No protection was observed in non-reperfused post-infarcted hearts. The respiratory control index of mitochondria was significantly reduced in reperfused infarcted hearts at 2-days with no effect at 28-days post-infarction on reperfused and non-reperfused hearts. Likewise, only a minor increase in reactive oxygen species production was observed at 2-days in non-reperfused post-infarcted hearts. Conclusion: This study demonstrates that CyP-D inhibition exerts cardioprotective effects in reperfused but not in non-reperfused infarcted hearts of female rats, and the effects are observed only during acute post-infarction injury. |
| doi_str_mv | 10.1159/000494006 |
| format | Article |
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Inhibition of cyclophilin-D (CyP-D), a key regulator of the mitochondrial permeability transition pore, has been shown to exert cardioprotective effects against ischemia-reperfusion injury on various animal models, mostly in males. However, failure of recent clinical trials requires a detailed elucidation of the cardioprotective efficacy of CyP-D inhibition. The aim of this study was to examine whether cardioprotective effects of sanglifehrin A, a potent inhibitor of CyP-D, on post-infarcted hearts depends on reperfusion. Methods: Acute or chronic myocardial infarction was induced by coronary artery ligation with/without subsequent reperfusion for 2 and 28 days in female Sprague-Dawley rats. Cardiac function was estimated by echocardiography. Oxygen consumption rates, ROS production, permeability transition pore opening, protein carbonylation and respiratory supercomplexes were analyzed in isolated cardiac mitochondria. Results: Sanglifehrin A significantly improved cardiac function of reperfused hearts at 2 days but failed to protect after 28 days. No protection was observed in non-reperfused post-infarcted hearts. The respiratory control index of mitochondria was significantly reduced in reperfused infarcted hearts at 2-days with no effect at 28-days post-infarction on reperfused and non-reperfused hearts. Likewise, only a minor increase in reactive oxygen species production was observed at 2-days in non-reperfused post-infarcted hearts. Conclusion: This study demonstrates that CyP-D inhibition exerts cardioprotective effects in reperfused but not in non-reperfused infarcted hearts of female rats, and the effects are observed only during acute post-infarction injury.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000494006</identifier><identifier>PMID: 30282073</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Acetylation ; Acute Disease ; Alcohol ; Animals ; Autophagy ; Cardiac function ; Cardioprotection ; Cardiovascular disease ; Chronic Disease ; Coronary vessels ; Cyclophilin D ; Cyclophilins - antagonists & inhibitors ; Cyclophilins - metabolism ; Design of experiments ; Echocardiography ; Estrogens ; Female ; Heart - drug effects ; Heart attacks ; Ischemia ; Laboratory animals ; Lactones - pharmacology ; Metabolism ; Mitochondria ; Mitochondria, Heart - metabolism ; Mitochondrial Membrane Transport Proteins - metabolism ; Mitochondrial permeability transition ; Mitochondrial Permeability Transition Pore ; Myocardial infarction ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocardial Infarction - veterinary ; Original Paper ; Ostomy ; Oxygen Consumption - drug effects ; Peptidyl-Prolyl Isomerase F ; Permeability ; Rats ; Rats, Sprague-Dawley ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Reperfusion ; Rodents ; Sanglifehrin A ; Sirtuins - metabolism ; Spiro Compounds - pharmacology</subject><ispartof>Cellular physiology and biochemistry, 2018-01, Vol.50 (1), p.288-303</ispartof><rights>2018 The Author(s). Published by S. Karger AG, Basel</rights><rights>2018 The Author(s). Published by S. Karger AG, Basel.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-6585159d4dce6fea367eda6d95b37cfd7952e8d160719615851525d087015bd33</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,860,881,2096,27612,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30282073$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Parodi-Rullán, Rebecca M.</creatorcontrib><creatorcontrib>Soto-Prado, Jadira</creatorcontrib><creatorcontrib>Vega-Lugo, Jesús</creatorcontrib><creatorcontrib>Chapa-Dubocq, Xavier</creatorcontrib><creatorcontrib>Díaz-Cordero, Sara I.</creatorcontrib><creatorcontrib>Javadov, Sabzali </creatorcontrib><title>Divergent Effects of Cyclophilin-D Inhibition on the Female Rat Heart: Acute Versus Chronic Post-Myocardial Infarction</title><title>Cellular physiology and biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Background/Aims: The mitochondrial permeability transition pore opening plays a critical role in the pathogenesis of myocardial infarction. Inhibition of cyclophilin-D (CyP-D), a key regulator of the mitochondrial permeability transition pore, has been shown to exert cardioprotective effects against ischemia-reperfusion injury on various animal models, mostly in males. However, failure of recent clinical trials requires a detailed elucidation of the cardioprotective efficacy of CyP-D inhibition. The aim of this study was to examine whether cardioprotective effects of sanglifehrin A, a potent inhibitor of CyP-D, on post-infarcted hearts depends on reperfusion. Methods: Acute or chronic myocardial infarction was induced by coronary artery ligation with/without subsequent reperfusion for 2 and 28 days in female Sprague-Dawley rats. Cardiac function was estimated by echocardiography. Oxygen consumption rates, ROS production, permeability transition pore opening, protein carbonylation and respiratory supercomplexes were analyzed in isolated cardiac mitochondria. Results: Sanglifehrin A significantly improved cardiac function of reperfused hearts at 2 days but failed to protect after 28 days. No protection was observed in non-reperfused post-infarcted hearts. The respiratory control index of mitochondria was significantly reduced in reperfused infarcted hearts at 2-days with no effect at 28-days post-infarction on reperfused and non-reperfused hearts. Likewise, only a minor increase in reactive oxygen species production was observed at 2-days in non-reperfused post-infarcted hearts. Conclusion: This study demonstrates that CyP-D inhibition exerts cardioprotective effects in reperfused but not in non-reperfused infarcted hearts of female rats, and the effects are observed only during acute post-infarction injury.</description><subject>Acetylation</subject><subject>Acute Disease</subject><subject>Alcohol</subject><subject>Animals</subject><subject>Autophagy</subject><subject>Cardiac function</subject><subject>Cardioprotection</subject><subject>Cardiovascular disease</subject><subject>Chronic Disease</subject><subject>Coronary vessels</subject><subject>Cyclophilin D</subject><subject>Cyclophilins - antagonists & inhibitors</subject><subject>Cyclophilins - metabolism</subject><subject>Design of experiments</subject><subject>Echocardiography</subject><subject>Estrogens</subject><subject>Female</subject><subject>Heart - drug effects</subject><subject>Heart attacks</subject><subject>Ischemia</subject><subject>Laboratory animals</subject><subject>Lactones - pharmacology</subject><subject>Metabolism</subject><subject>Mitochondria</subject><subject>Mitochondria, Heart - metabolism</subject><subject>Mitochondrial Membrane Transport Proteins - metabolism</subject><subject>Mitochondrial permeability transition</subject><subject>Mitochondrial Permeability Transition Pore</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - veterinary</subject><subject>Original Paper</subject><subject>Ostomy</subject><subject>Oxygen Consumption - drug effects</subject><subject>Peptidyl-Prolyl Isomerase F</subject><subject>Permeability</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Reperfusion</subject><subject>Rodents</subject><subject>Sanglifehrin A</subject><subject>Sirtuins - metabolism</subject><subject>Spiro Compounds - pharmacology</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNpdks1rFDEYhwdRbK0evIsEvOhhNMlMvnoQyra1CxVF1GvIJO_sZp2drElmYf970-66WCGQrycP7xt-VfWS4PeEMPUBY9yqFmP-qDolLSW1EkI-LmtMWC2VFCfVs5RWuGyFok-rkwZTSbFoTqvtpd9CXMCY0VXfg80JhR7NdnYIm6Uf_Fhfovm49J3PPoyojLwEdA1rMwD6ZjK6ARPzObqwUwb0E2KaEpotYxi9RV9DyvXnXbAmOm-GIupNtHei59WT3gwJXhzms-rH9dX32U19--XTfHZxW9tW4VxzJllp0LXOAu_BNFyAM9wp1jXC9k4oRkE6wrEgipN7mjKHpSitdq5pzqr53uuCWelN9GsTdzoYr-8PQlzoUr63A2guqRCA20YS1pbvMcQxKUBR6Nq-a2xxfdy7NlO3hlLRmKMZHkgf3ox-qRdhqzlthVCkCN4eBDH8niBlvfbJwjCYEcKUNCWEE8oxkwV98x-6ClMcy1dp2mAipVItK9S7PWVjSClCfyyGYH2XDH1MRmFf_1v9kfwbhQK82gO_TMlDPAKH938AbES7BA</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Parodi-Rullán, Rebecca M.</creator><creator>Soto-Prado, Jadira</creator><creator>Vega-Lugo, Jesús</creator><creator>Chapa-Dubocq, Xavier</creator><creator>Díaz-Cordero, Sara I.</creator><creator>Javadov, Sabzali </creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20180101</creationdate><title>Divergent Effects of Cyclophilin-D Inhibition on the Female Rat Heart: Acute Versus Chronic Post-Myocardial Infarction</title><author>Parodi-Rullán, Rebecca M. ; Soto-Prado, Jadira ; Vega-Lugo, Jesús ; Chapa-Dubocq, Xavier ; Díaz-Cordero, Sara I. ; Javadov, Sabzali </author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c490t-6585159d4dce6fea367eda6d95b37cfd7952e8d160719615851525d087015bd33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Acetylation</topic><topic>Acute Disease</topic><topic>Alcohol</topic><topic>Animals</topic><topic>Autophagy</topic><topic>Cardiac function</topic><topic>Cardioprotection</topic><topic>Cardiovascular disease</topic><topic>Chronic Disease</topic><topic>Coronary vessels</topic><topic>Cyclophilin D</topic><topic>Cyclophilins - antagonists & inhibitors</topic><topic>Cyclophilins - metabolism</topic><topic>Design of experiments</topic><topic>Echocardiography</topic><topic>Estrogens</topic><topic>Female</topic><topic>Heart - drug effects</topic><topic>Heart attacks</topic><topic>Ischemia</topic><topic>Laboratory animals</topic><topic>Lactones - pharmacology</topic><topic>Metabolism</topic><topic>Mitochondria</topic><topic>Mitochondria, Heart - metabolism</topic><topic>Mitochondrial Membrane Transport Proteins - metabolism</topic><topic>Mitochondrial permeability transition</topic><topic>Mitochondrial Permeability Transition Pore</topic><topic>Myocardial infarction</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Infarction - veterinary</topic><topic>Original Paper</topic><topic>Ostomy</topic><topic>Oxygen Consumption - drug effects</topic><topic>Peptidyl-Prolyl Isomerase F</topic><topic>Permeability</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Reperfusion</topic><topic>Rodents</topic><topic>Sanglifehrin A</topic><topic>Sirtuins - metabolism</topic><topic>Spiro Compounds - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Parodi-Rullán, Rebecca M.</creatorcontrib><creatorcontrib>Soto-Prado, Jadira</creatorcontrib><creatorcontrib>Vega-Lugo, Jesús</creatorcontrib><creatorcontrib>Chapa-Dubocq, Xavier</creatorcontrib><creatorcontrib>Díaz-Cordero, Sara I.</creatorcontrib><creatorcontrib>Javadov, Sabzali </creatorcontrib><collection>Karger Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular physiology and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Parodi-Rullán, Rebecca M.</au><au>Soto-Prado, Jadira</au><au>Vega-Lugo, Jesús</au><au>Chapa-Dubocq, Xavier</au><au>Díaz-Cordero, Sara I.</au><au>Javadov, Sabzali </au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Divergent Effects of Cyclophilin-D Inhibition on the Female Rat Heart: Acute Versus Chronic Post-Myocardial Infarction</atitle><jtitle>Cellular physiology and biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>50</volume><issue>1</issue><spage>288</spage><epage>303</epage><pages>288-303</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Background/Aims: The mitochondrial permeability transition pore opening plays a critical role in the pathogenesis of myocardial infarction. Inhibition of cyclophilin-D (CyP-D), a key regulator of the mitochondrial permeability transition pore, has been shown to exert cardioprotective effects against ischemia-reperfusion injury on various animal models, mostly in males. However, failure of recent clinical trials requires a detailed elucidation of the cardioprotective efficacy of CyP-D inhibition. The aim of this study was to examine whether cardioprotective effects of sanglifehrin A, a potent inhibitor of CyP-D, on post-infarcted hearts depends on reperfusion. Methods: Acute or chronic myocardial infarction was induced by coronary artery ligation with/without subsequent reperfusion for 2 and 28 days in female Sprague-Dawley rats. Cardiac function was estimated by echocardiography. Oxygen consumption rates, ROS production, permeability transition pore opening, protein carbonylation and respiratory supercomplexes were analyzed in isolated cardiac mitochondria. Results: Sanglifehrin A significantly improved cardiac function of reperfused hearts at 2 days but failed to protect after 28 days. No protection was observed in non-reperfused post-infarcted hearts. The respiratory control index of mitochondria was significantly reduced in reperfused infarcted hearts at 2-days with no effect at 28-days post-infarction on reperfused and non-reperfused hearts. Likewise, only a minor increase in reactive oxygen species production was observed at 2-days in non-reperfused post-infarcted hearts. Conclusion: This study demonstrates that CyP-D inhibition exerts cardioprotective effects in reperfused but not in non-reperfused infarcted hearts of female rats, and the effects are observed only during acute post-infarction injury.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>30282073</pmid><doi>10.1159/000494006</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acetylation Acute Disease Alcohol Animals Autophagy Cardiac function Cardioprotection Cardiovascular disease Chronic Disease Coronary vessels Cyclophilin D Cyclophilins - antagonists & inhibitors Cyclophilins - metabolism Design of experiments Echocardiography Estrogens Female Heart - drug effects Heart attacks Ischemia Laboratory animals Lactones - pharmacology Metabolism Mitochondria Mitochondria, Heart - metabolism Mitochondrial Membrane Transport Proteins - metabolism Mitochondrial permeability transition Mitochondrial Permeability Transition Pore Myocardial infarction Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocardial Infarction - veterinary Original Paper Ostomy Oxygen Consumption - drug effects Peptidyl-Prolyl Isomerase F Permeability Rats Rats, Sprague-Dawley Reactive oxygen species Reactive Oxygen Species - metabolism Reperfusion Rodents Sanglifehrin A Sirtuins - metabolism Spiro Compounds - pharmacology |
| title | Divergent Effects of Cyclophilin-D Inhibition on the Female Rat Heart: Acute Versus Chronic Post-Myocardial Infarction |
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