miR-613 suppresses ischemia-reperfusion-induced cardiomyocyte apoptosis by targeting the programmed cell death 10 gene
MicroRNAs (miRNAs) are important gene regulators in both biological and pathological processes, including myocardial ischemia/reperfusion (I/R) injury. This study investigated the effect of miR-613 on I/R-induced cardiomyocyte apoptosis and its molecular mechanism of action. Hypoxia/reoxygenation (H...
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| Veröffentlicht in: | BioScience Trends 2016, Vol.10(4), pp.251-257 |
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| description | MicroRNAs (miRNAs) are important gene regulators in both biological and pathological processes, including myocardial ischemia/reperfusion (I/R) injury. This study investigated the effect of miR-613 on I/R-induced cardiomyocyte apoptosis and its molecular mechanism of action. Hypoxia/reoxygenation (H/R) significantly increased the release of lactate dehydrogenase (LDH), levels of malondialdehyde (MDA), and cardiomyocyte apoptosis, but these effects were attenuated by an miR-613 mimic. Programmed cell death 10 (PDCD10) was identified as a target gene of miR-613. miR-613 significantly increased the phosphorylation of Akt (p-Akt). An miR-613 mimic lowered the level of expression of pro-apoptotic proteins, C/EBP homologous protein (CHOP), and phosphorylated c-Jun N-terminal kinase (p-JNK), and it up-regulated the expression of the anti-apoptotic protein B-cell lymphoma-2 (Bcl-2). All of these effects were reversed by restoration of PDCD10. Taken together, the current findings indicate that miR-613 inhibits I/R-induced cardiomyocyte apoptosis by targeting PDCD10 by regulating the PI3K/AKT signaling pathway. |
| doi_str_mv | 10.5582/bst.2016.01122 |
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This study investigated the effect of miR-613 on I/R-induced cardiomyocyte apoptosis and its molecular mechanism of action. Hypoxia/reoxygenation (H/R) significantly increased the release of lactate dehydrogenase (LDH), levels of malondialdehyde (MDA), and cardiomyocyte apoptosis, but these effects were attenuated by an miR-613 mimic. Programmed cell death 10 (PDCD10) was identified as a target gene of miR-613. miR-613 significantly increased the phosphorylation of Akt (p-Akt). An miR-613 mimic lowered the level of expression of pro-apoptotic proteins, C/EBP homologous protein (CHOP), and phosphorylated c-Jun N-terminal kinase (p-JNK), and it up-regulated the expression of the anti-apoptotic protein B-cell lymphoma-2 (Bcl-2). All of these effects were reversed by restoration of PDCD10. Taken together, the current findings indicate that miR-613 inhibits I/R-induced cardiomyocyte apoptosis by targeting PDCD10 by regulating the PI3K/AKT signaling pathway.</description><identifier>ISSN: 1881-7815</identifier><identifier>EISSN: 1881-7823</identifier><identifier>DOI: 10.5582/bst.2016.01122</identifier><identifier>PMID: 27534371</identifier><language>eng</language><publisher>Japan: International Research and Cooperation Association for Bio & Socio-Sciences Advancement</publisher><subject>Apoptosis - genetics ; Apoptosis Regulatory Proteins - genetics ; Apoptosis Regulatory Proteins - metabolism ; Apoptosis Regulatory Proteins - physiology ; B-cell lymphoma-2 ; C/EBP homologous protein ; Cell Line ; Gene Expression Regulation ; Humans ; hypoxia/reoxygenation ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Membrane Proteins - physiology ; MicroRNAs - physiology ; miRNAs ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; PI3K/AKT ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins - metabolism ; Proto-Oncogene Proteins - physiology ; Proto-Oncogene Proteins c-akt ; Reperfusion Injury - genetics ; Signal Transduction</subject><ispartof>BioScience Trends, 2016, Vol.10(4), pp.251-257</ispartof><rights>2016 International Research and Cooperation Association for Bio & Socio-Sciences Advancement</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c543t-45cb14733699d12db57767896b2a41987c842a9cfa1c3ca6568edf94fed5dd003</citedby><cites>FETCH-LOGICAL-c543t-45cb14733699d12db57767896b2a41987c842a9cfa1c3ca6568edf94fed5dd003</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,1884,4025,27927,27928,27929</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27534371$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Zhenhua</creatorcontrib><creatorcontrib>Qi, Yujuan</creatorcontrib><creatorcontrib>Guo, Zhigang</creatorcontrib><creatorcontrib>Li, Peijun</creatorcontrib><creatorcontrib>Zhou, Ding</creatorcontrib><title>miR-613 suppresses ischemia-reperfusion-induced cardiomyocyte apoptosis by targeting the programmed cell death 10 gene</title><title>BioScience Trends</title><addtitle>BST</addtitle><description>MicroRNAs (miRNAs) are important gene regulators in both biological and pathological processes, including myocardial ischemia/reperfusion (I/R) injury. This study investigated the effect of miR-613 on I/R-induced cardiomyocyte apoptosis and its molecular mechanism of action. Hypoxia/reoxygenation (H/R) significantly increased the release of lactate dehydrogenase (LDH), levels of malondialdehyde (MDA), and cardiomyocyte apoptosis, but these effects were attenuated by an miR-613 mimic. Programmed cell death 10 (PDCD10) was identified as a target gene of miR-613. miR-613 significantly increased the phosphorylation of Akt (p-Akt). An miR-613 mimic lowered the level of expression of pro-apoptotic proteins, C/EBP homologous protein (CHOP), and phosphorylated c-Jun N-terminal kinase (p-JNK), and it up-regulated the expression of the anti-apoptotic protein B-cell lymphoma-2 (Bcl-2). All of these effects were reversed by restoration of PDCD10. Taken together, the current findings indicate that miR-613 inhibits I/R-induced cardiomyocyte apoptosis by targeting PDCD10 by regulating the PI3K/AKT signaling pathway.</description><subject>Apoptosis - genetics</subject><subject>Apoptosis Regulatory Proteins - genetics</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Apoptosis Regulatory Proteins - physiology</subject><subject>B-cell lymphoma-2</subject><subject>C/EBP homologous protein</subject><subject>Cell Line</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>hypoxia/reoxygenation</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Membrane Proteins - physiology</subject><subject>MicroRNAs - physiology</subject><subject>miRNAs</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>PI3K/AKT</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Proto-Oncogene Proteins - physiology</subject><subject>Proto-Oncogene Proteins c-akt</subject><subject>Reperfusion Injury - genetics</subject><subject>Signal Transduction</subject><issn>1881-7815</issn><issn>1881-7823</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE2LFDEQhoMo7rLu1aPk6KXHVNL56KOsrgoLgug5pJPqnizTHyZpYf69mZ11zCEpyFMvVQ8hb4HtpDT8Q5_LjjNQOwbA-QtyDcZAow0XLy81yCtym_Mjq0cqMFq9JldcS9EKDdfkzxR_NAoEzdu6JswZM43Z73GKrkm4Yhq2HJe5iXPYPAbqXQpxmY6LPxakbl3WsuSYaX-kxaURS5xHWvZI17SMyU3TqQcPBxrQlT0FRkec8Q15NbhDxtvn94b8uv_88-5r8_D9y7e7jw-Nl60oTSt9D60WQnVdAB56qbXSplM9dy10RnvTctf5wYEX3impDIahawcMMgTGxA15f86t0_zeMBc71e3qOG7GZcsWDGjGpRKqorsz6tOSc8LBrilOLh0tMHvSbatue9Jtn3TXhnfP2Vtft7zg_-RW4NMZeMzFjXgBXCrRH_Apr2a3p-t_7uXb712yOIu_5jSUWw</recordid><startdate>2016</startdate><enddate>2016</enddate><creator>Wu, Zhenhua</creator><creator>Qi, Yujuan</creator><creator>Guo, Zhigang</creator><creator>Li, Peijun</creator><creator>Zhou, Ding</creator><general>International Research and Cooperation Association for Bio & Socio-Sciences Advancement</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></search><sort><creationdate>2016</creationdate><title>miR-613 suppresses ischemia-reperfusion-induced cardiomyocyte apoptosis by targeting the programmed cell death 10 gene</title><author>Wu, Zhenhua ; Qi, Yujuan ; Guo, Zhigang ; Li, Peijun ; Zhou, Ding</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c543t-45cb14733699d12db57767896b2a41987c842a9cfa1c3ca6568edf94fed5dd003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Apoptosis - genetics</topic><topic>Apoptosis Regulatory Proteins - genetics</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Apoptosis Regulatory Proteins - physiology</topic><topic>B-cell lymphoma-2</topic><topic>C/EBP homologous protein</topic><topic>Cell Line</topic><topic>Gene Expression Regulation</topic><topic>Humans</topic><topic>hypoxia/reoxygenation</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Membrane Proteins - physiology</topic><topic>MicroRNAs - physiology</topic><topic>miRNAs</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - pathology</topic><topic>PI3K/AKT</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Proto-Oncogene Proteins - physiology</topic><topic>Proto-Oncogene Proteins c-akt</topic><topic>Reperfusion Injury - genetics</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Zhenhua</creatorcontrib><creatorcontrib>Qi, Yujuan</creatorcontrib><creatorcontrib>Guo, Zhigang</creatorcontrib><creatorcontrib>Li, Peijun</creatorcontrib><creatorcontrib>Zhou, Ding</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>BioScience Trends</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Zhenhua</au><au>Qi, Yujuan</au><au>Guo, Zhigang</au><au>Li, Peijun</au><au>Zhou, Ding</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-613 suppresses ischemia-reperfusion-induced cardiomyocyte apoptosis by targeting the programmed cell death 10 gene</atitle><jtitle>BioScience Trends</jtitle><addtitle>BST</addtitle><date>2016</date><risdate>2016</risdate><volume>10</volume><issue>4</issue><spage>251</spage><epage>257</epage><pages>251-257</pages><issn>1881-7815</issn><eissn>1881-7823</eissn><abstract>MicroRNAs (miRNAs) are important gene regulators in both biological and pathological processes, including myocardial ischemia/reperfusion (I/R) injury. This study investigated the effect of miR-613 on I/R-induced cardiomyocyte apoptosis and its molecular mechanism of action. Hypoxia/reoxygenation (H/R) significantly increased the release of lactate dehydrogenase (LDH), levels of malondialdehyde (MDA), and cardiomyocyte apoptosis, but these effects were attenuated by an miR-613 mimic. Programmed cell death 10 (PDCD10) was identified as a target gene of miR-613. miR-613 significantly increased the phosphorylation of Akt (p-Akt). An miR-613 mimic lowered the level of expression of pro-apoptotic proteins, C/EBP homologous protein (CHOP), and phosphorylated c-Jun N-terminal kinase (p-JNK), and it up-regulated the expression of the anti-apoptotic protein B-cell lymphoma-2 (Bcl-2). All of these effects were reversed by restoration of PDCD10. Taken together, the current findings indicate that miR-613 inhibits I/R-induced cardiomyocyte apoptosis by targeting PDCD10 by regulating the PI3K/AKT signaling pathway.</abstract><cop>Japan</cop><pub>International Research and Cooperation Association for Bio & Socio-Sciences Advancement</pub><pmid>27534371</pmid><doi>10.5582/bst.2016.01122</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; J-STAGE (Japan Science & Technology Information Aggregator, Electronic) Freely Available Titles - Japanese |
| subjects | Apoptosis - genetics Apoptosis Regulatory Proteins - genetics Apoptosis Regulatory Proteins - metabolism Apoptosis Regulatory Proteins - physiology B-cell lymphoma-2 C/EBP homologous protein Cell Line Gene Expression Regulation Humans hypoxia/reoxygenation Membrane Proteins - genetics Membrane Proteins - metabolism Membrane Proteins - physiology MicroRNAs - physiology miRNAs Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology PI3K/AKT Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins - physiology Proto-Oncogene Proteins c-akt Reperfusion Injury - genetics Signal Transduction |
| title | miR-613 suppresses ischemia-reperfusion-induced cardiomyocyte apoptosis by targeting the programmed cell death 10 gene |
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