Leucine induces cardioprotection in vitro by promoting mitochondrial function via mTOR and Opa-1 signaling
Coronary heart disease is a major global health concern. Further, severity of this condition is greatly influenced by myocardial ischemia/reperfusion (I/R) injury. Branched-chain amino acids (BCAAs) have cardioprotective effects against I/R via mammalian target of rapamycin (mTOR) activity, wherein...
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| creator | Morio, Atsushi Tsutsumi, Rie Kondo, Takashi Miyoshi, Hirotsugu Kato, Takahiro Narasaki, Soshi Satomi, Shiho Nakaya, Erika Kuroda, Masashi Sakaue, Hiroshi Kitamura, Tadahiro Tsutsumi, Yasuo M. |
| description | Coronary heart disease is a major global health concern. Further, severity of this condition is greatly influenced by myocardial ischemia/reperfusion (I/R) injury. Branched-chain amino acids (BCAAs) have cardioprotective effects against I/R via mammalian target of rapamycin (mTOR) activity, wherein Leu is considered to particularly regulate mTOR activation. However, the mechanism underlying cardioprotective effects of Leu via mTOR activity is not fully elucidated. Here, we aimed to study the signaling pathway of cardioprotection and mitochondrial function induced by Leu treatment.
Cardiac myocytes isolated from adult male Wistar rats were incubated and exposed to simulated I/R (SI/R) injury by replacing the air content. Cardiac myocytes were treated with Leu and subsequently, their survival rate was calculated. To elucidate the signaling pathway and mitochondrial function, immunoblots and mitochondrial permeability transition pore were examined. Cell survival rate was decreased with SI/R but improved by 160 μM Leu (38.5 ± 3.6% vs. 64.5 ± 4.2%, respectively, p |
| doi_str_mv | 10.1016/j.numecd.2021.06.025 |
| format | Article |
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Cardiac myocytes isolated from adult male Wistar rats were incubated and exposed to simulated I/R (SI/R) injury by replacing the air content. Cardiac myocytes were treated with Leu and subsequently, their survival rate was calculated. To elucidate the signaling pathway and mitochondrial function, immunoblots and mitochondrial permeability transition pore were examined. Cell survival rate was decreased with SI/R but improved by 160 μM Leu (38.5 ± 3.6% vs. 64.5 ± 4.2%, respectively, p < 0.001). Although rapamycin (mTOR inhibitor) prevented this cardioprotective effect induced by Leu, wortmannin (PI3K inhibitor) did not interfere with this effect. In addition, we indicated that overexpression of Opa-1 and mitochondrial function are ameliorated via Leu-induced mitochondrial biogenesis. In contrast, knockdown of Opa-1 suppressed Leu-induced cardioprotection.
Leu treatment is critical in rendering a cardioprotective effect exhibited by BCAAs via mTOR signaling. Furthermore, Leu improved mitochondrial function.
•Leucine (Leu, 160 μM) improved survival rate of cardiomyocytes in vitro.•Rapamycin (mTOR inhibitor) prevented the cardioprotective effect induced by Leu.•Wortmannin (PI3K inhibitor) did not hinder this effect induced by Leu.•Leu-induced mitochondrial biogenesis improved mitochondrial function.•Leu treatment is critical in cardioprotection via mTOR signaling.</description><identifier>ISSN: 0939-4753</identifier><identifier>EISSN: 1590-3729</identifier><identifier>DOI: 10.1016/j.numecd.2021.06.025</identifier><identifier>PMID: 34362635</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; BCAAs ; Cell Survival - drug effects ; Cells, Cultured ; GTP Phosphohydrolases - genetics ; GTP Phosphohydrolases - metabolism ; Ischemia-reperfusion ; Leucine ; Leucine - pharmacology ; Male ; Mitochondria, Heart - drug effects ; Mitochondria, Heart - enzymology ; Mitochondria, Heart - genetics ; Mitochondria, Heart - pathology ; Mitochondrial Dynamics - drug effects ; Mitochondrial function ; mTOR ; Myocardial Reperfusion Injury - enzymology ; Myocardial Reperfusion Injury - genetics ; Myocardial Reperfusion Injury - pathology ; Myocardial Reperfusion Injury - prevention & control ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - enzymology ; Myocytes, Cardiac - pathology ; Opa-1 ; Organelle Biogenesis ; Rats ; Rats, Wistar ; Signal Transduction ; TOR Serine-Threonine Kinases - metabolism</subject><ispartof>Nutrition, metabolism, and cardiovascular diseases, 2021-09, Vol.31 (10), p.2979-2986</ispartof><rights>2021 The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University</rights><rights>Copyright © 2021 The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-395adccb226f7714f05a909418e65f13cd53bb9c3636d4577aa7a6f5ae03aa7d3</citedby><cites>FETCH-LOGICAL-c408t-395adccb226f7714f05a909418e65f13cd53bb9c3636d4577aa7a6f5ae03aa7d3</cites><orcidid>0000-0001-9360-9437 ; 0000-0001-9182-0394 ; 0000-0002-1375-5344 ; 0000-0002-8330-4290 ; 0000-0002-9838-078X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0939475321003227$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34362635$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Morio, Atsushi</creatorcontrib><creatorcontrib>Tsutsumi, Rie</creatorcontrib><creatorcontrib>Kondo, Takashi</creatorcontrib><creatorcontrib>Miyoshi, Hirotsugu</creatorcontrib><creatorcontrib>Kato, Takahiro</creatorcontrib><creatorcontrib>Narasaki, Soshi</creatorcontrib><creatorcontrib>Satomi, Shiho</creatorcontrib><creatorcontrib>Nakaya, Erika</creatorcontrib><creatorcontrib>Kuroda, Masashi</creatorcontrib><creatorcontrib>Sakaue, Hiroshi</creatorcontrib><creatorcontrib>Kitamura, Tadahiro</creatorcontrib><creatorcontrib>Tsutsumi, Yasuo M.</creatorcontrib><title>Leucine induces cardioprotection in vitro by promoting mitochondrial function via mTOR and Opa-1 signaling</title><title>Nutrition, metabolism, and cardiovascular diseases</title><addtitle>Nutr Metab Cardiovasc Dis</addtitle><description>Coronary heart disease is a major global health concern. Further, severity of this condition is greatly influenced by myocardial ischemia/reperfusion (I/R) injury. Branched-chain amino acids (BCAAs) have cardioprotective effects against I/R via mammalian target of rapamycin (mTOR) activity, wherein Leu is considered to particularly regulate mTOR activation. However, the mechanism underlying cardioprotective effects of Leu via mTOR activity is not fully elucidated. Here, we aimed to study the signaling pathway of cardioprotection and mitochondrial function induced by Leu treatment.
Cardiac myocytes isolated from adult male Wistar rats were incubated and exposed to simulated I/R (SI/R) injury by replacing the air content. Cardiac myocytes were treated with Leu and subsequently, their survival rate was calculated. To elucidate the signaling pathway and mitochondrial function, immunoblots and mitochondrial permeability transition pore were examined. Cell survival rate was decreased with SI/R but improved by 160 μM Leu (38.5 ± 3.6% vs. 64.5 ± 4.2%, respectively, p < 0.001). Although rapamycin (mTOR inhibitor) prevented this cardioprotective effect induced by Leu, wortmannin (PI3K inhibitor) did not interfere with this effect. In addition, we indicated that overexpression of Opa-1 and mitochondrial function are ameliorated via Leu-induced mitochondrial biogenesis. In contrast, knockdown of Opa-1 suppressed Leu-induced cardioprotection.
Leu treatment is critical in rendering a cardioprotective effect exhibited by BCAAs via mTOR signaling. Furthermore, Leu improved mitochondrial function.
•Leucine (Leu, 160 μM) improved survival rate of cardiomyocytes in vitro.•Rapamycin (mTOR inhibitor) prevented the cardioprotective effect induced by Leu.•Wortmannin (PI3K inhibitor) did not hinder this effect induced by Leu.•Leu-induced mitochondrial biogenesis improved mitochondrial function.•Leu treatment is critical in cardioprotection via mTOR signaling.</description><subject>Animals</subject><subject>BCAAs</subject><subject>Cell Survival - drug effects</subject><subject>Cells, Cultured</subject><subject>GTP Phosphohydrolases - genetics</subject><subject>GTP Phosphohydrolases - metabolism</subject><subject>Ischemia-reperfusion</subject><subject>Leucine</subject><subject>Leucine - pharmacology</subject><subject>Male</subject><subject>Mitochondria, Heart - drug effects</subject><subject>Mitochondria, Heart - enzymology</subject><subject>Mitochondria, Heart - genetics</subject><subject>Mitochondria, Heart - pathology</subject><subject>Mitochondrial Dynamics - drug effects</subject><subject>Mitochondrial function</subject><subject>mTOR</subject><subject>Myocardial Reperfusion Injury - enzymology</subject><subject>Myocardial Reperfusion Injury - genetics</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocardial Reperfusion Injury - prevention & control</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - enzymology</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Opa-1</subject><subject>Organelle Biogenesis</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Signal Transduction</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><issn>0939-4753</issn><issn>1590-3729</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kN9O5CAUh8lGszM77huYDZfetEIpdLgxMcb9k0wyiRmvCYVTl7GFWWgn8W18ln0yMVUvvYJwvh_nnA-hc0pKSqi43Jd-GsDYsiIVLYkoScW_oCXlkhSsqeQJWhLJZFE3nC3Qt5T2hLCGsPorWrCaiUowvkSPG5iM84Cdt5OBhI2O1oVDDCOY0QWfC_-fj26MAbdPOL8PYXT-AQ9uDOZv8DY63eNu8jN9dBoPu-0d1t7i7UEXFCf34HWfM2fotNN9gu9v5wrd_7zd3fwuNttff26uN4WpyXosmOTaGtNWleiahtYd4VoSWdM1CN5RZixnbSsNE0zYmjeN1o0WHddAWL5atkIX87952n8TpFENLhnoe-0hTElVnMssIIvKaD2jJoaUInTqEN2g45OiRL1qVns1a1avmhURKmvOsR9vHaZ2APsReveagasZgLzn0UFUyTjwBqyL2auywX3e4QUtm5Jz</recordid><startdate>20210922</startdate><enddate>20210922</enddate><creator>Morio, Atsushi</creator><creator>Tsutsumi, Rie</creator><creator>Kondo, Takashi</creator><creator>Miyoshi, Hirotsugu</creator><creator>Kato, Takahiro</creator><creator>Narasaki, Soshi</creator><creator>Satomi, Shiho</creator><creator>Nakaya, Erika</creator><creator>Kuroda, Masashi</creator><creator>Sakaue, Hiroshi</creator><creator>Kitamura, Tadahiro</creator><creator>Tsutsumi, Yasuo M.</creator><general>Elsevier B.V</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><orcidid>https://orcid.org/0000-0001-9360-9437</orcidid><orcidid>https://orcid.org/0000-0001-9182-0394</orcidid><orcidid>https://orcid.org/0000-0002-1375-5344</orcidid><orcidid>https://orcid.org/0000-0002-8330-4290</orcidid><orcidid>https://orcid.org/0000-0002-9838-078X</orcidid></search><sort><creationdate>20210922</creationdate><title>Leucine induces cardioprotection in vitro by promoting mitochondrial function via mTOR and Opa-1 signaling</title><author>Morio, Atsushi ; Tsutsumi, Rie ; Kondo, Takashi ; Miyoshi, Hirotsugu ; Kato, Takahiro ; Narasaki, Soshi ; Satomi, Shiho ; Nakaya, Erika ; Kuroda, Masashi ; Sakaue, Hiroshi ; Kitamura, Tadahiro ; Tsutsumi, Yasuo M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-395adccb226f7714f05a909418e65f13cd53bb9c3636d4577aa7a6f5ae03aa7d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>BCAAs</topic><topic>Cell Survival - drug effects</topic><topic>Cells, Cultured</topic><topic>GTP Phosphohydrolases - genetics</topic><topic>GTP Phosphohydrolases - metabolism</topic><topic>Ischemia-reperfusion</topic><topic>Leucine</topic><topic>Leucine - pharmacology</topic><topic>Male</topic><topic>Mitochondria, Heart - drug effects</topic><topic>Mitochondria, Heart - enzymology</topic><topic>Mitochondria, Heart - genetics</topic><topic>Mitochondria, Heart - pathology</topic><topic>Mitochondrial Dynamics - drug effects</topic><topic>Mitochondrial function</topic><topic>mTOR</topic><topic>Myocardial Reperfusion Injury - enzymology</topic><topic>Myocardial Reperfusion Injury - genetics</topic><topic>Myocardial Reperfusion Injury - pathology</topic><topic>Myocardial Reperfusion Injury - prevention & control</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - enzymology</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Opa-1</topic><topic>Organelle Biogenesis</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Signal Transduction</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Morio, Atsushi</creatorcontrib><creatorcontrib>Tsutsumi, Rie</creatorcontrib><creatorcontrib>Kondo, Takashi</creatorcontrib><creatorcontrib>Miyoshi, Hirotsugu</creatorcontrib><creatorcontrib>Kato, Takahiro</creatorcontrib><creatorcontrib>Narasaki, Soshi</creatorcontrib><creatorcontrib>Satomi, Shiho</creatorcontrib><creatorcontrib>Nakaya, Erika</creatorcontrib><creatorcontrib>Kuroda, Masashi</creatorcontrib><creatorcontrib>Sakaue, Hiroshi</creatorcontrib><creatorcontrib>Kitamura, Tadahiro</creatorcontrib><creatorcontrib>Tsutsumi, Yasuo M.</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><jtitle>Nutrition, metabolism, and cardiovascular diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Morio, Atsushi</au><au>Tsutsumi, Rie</au><au>Kondo, Takashi</au><au>Miyoshi, Hirotsugu</au><au>Kato, Takahiro</au><au>Narasaki, Soshi</au><au>Satomi, Shiho</au><au>Nakaya, Erika</au><au>Kuroda, Masashi</au><au>Sakaue, Hiroshi</au><au>Kitamura, Tadahiro</au><au>Tsutsumi, Yasuo M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Leucine induces cardioprotection in vitro by promoting mitochondrial function via mTOR and Opa-1 signaling</atitle><jtitle>Nutrition, metabolism, and cardiovascular diseases</jtitle><addtitle>Nutr Metab Cardiovasc Dis</addtitle><date>2021-09-22</date><risdate>2021</risdate><volume>31</volume><issue>10</issue><spage>2979</spage><epage>2986</epage><pages>2979-2986</pages><issn>0939-4753</issn><eissn>1590-3729</eissn><abstract>Coronary heart disease is a major global health concern. Further, severity of this condition is greatly influenced by myocardial ischemia/reperfusion (I/R) injury. Branched-chain amino acids (BCAAs) have cardioprotective effects against I/R via mammalian target of rapamycin (mTOR) activity, wherein Leu is considered to particularly regulate mTOR activation. However, the mechanism underlying cardioprotective effects of Leu via mTOR activity is not fully elucidated. Here, we aimed to study the signaling pathway of cardioprotection and mitochondrial function induced by Leu treatment.
Cardiac myocytes isolated from adult male Wistar rats were incubated and exposed to simulated I/R (SI/R) injury by replacing the air content. Cardiac myocytes were treated with Leu and subsequently, their survival rate was calculated. To elucidate the signaling pathway and mitochondrial function, immunoblots and mitochondrial permeability transition pore were examined. Cell survival rate was decreased with SI/R but improved by 160 μM Leu (38.5 ± 3.6% vs. 64.5 ± 4.2%, respectively, p < 0.001). Although rapamycin (mTOR inhibitor) prevented this cardioprotective effect induced by Leu, wortmannin (PI3K inhibitor) did not interfere with this effect. In addition, we indicated that overexpression of Opa-1 and mitochondrial function are ameliorated via Leu-induced mitochondrial biogenesis. In contrast, knockdown of Opa-1 suppressed Leu-induced cardioprotection.
Leu treatment is critical in rendering a cardioprotective effect exhibited by BCAAs via mTOR signaling. Furthermore, Leu improved mitochondrial function.
•Leucine (Leu, 160 μM) improved survival rate of cardiomyocytes in vitro.•Rapamycin (mTOR inhibitor) prevented the cardioprotective effect induced by Leu.•Wortmannin (PI3K inhibitor) did not hinder this effect induced by Leu.•Leu-induced mitochondrial biogenesis improved mitochondrial function.•Leu treatment is critical in cardioprotection via mTOR signaling.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>34362635</pmid><doi>10.1016/j.numecd.2021.06.025</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-9360-9437</orcidid><orcidid>https://orcid.org/0000-0001-9182-0394</orcidid><orcidid>https://orcid.org/0000-0002-1375-5344</orcidid><orcidid>https://orcid.org/0000-0002-8330-4290</orcidid><orcidid>https://orcid.org/0000-0002-9838-078X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals BCAAs Cell Survival - drug effects Cells, Cultured GTP Phosphohydrolases - genetics GTP Phosphohydrolases - metabolism Ischemia-reperfusion Leucine Leucine - pharmacology Male Mitochondria, Heart - drug effects Mitochondria, Heart - enzymology Mitochondria, Heart - genetics Mitochondria, Heart - pathology Mitochondrial Dynamics - drug effects Mitochondrial function mTOR Myocardial Reperfusion Injury - enzymology Myocardial Reperfusion Injury - genetics Myocardial Reperfusion Injury - pathology Myocardial Reperfusion Injury - prevention & control Myocytes, Cardiac - drug effects Myocytes, Cardiac - enzymology Myocytes, Cardiac - pathology Opa-1 Organelle Biogenesis Rats Rats, Wistar Signal Transduction TOR Serine-Threonine Kinases - metabolism |
| title | Leucine induces cardioprotection in vitro by promoting mitochondrial function via mTOR and Opa-1 signaling |
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