Role of microRNA-195 in cardiomyocyte apoptosis induced by myocardial ischaemia–reperfusion injury
This study aims to investigate microRNA-195 (miR-195) expression in myocardial ischaemia–reperfusion (I/R) injury and the roles of miR-195 in cardiomyocyte apoptosis though targeting Bcl-2. A mouse model of I/R injury was established. MiR-195 expression levels were detected by real-time quantitative...
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| Veröffentlicht in: | Journal of genetics 2016-03, Vol.95 (1), p.99-108 |
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| creator | GAO, CHANG-KUI LIU, HUI CUI, CHENG-JI LIANG, ZHAO-GUANG YAO, HONG TIAN, YE |
| description | This study aims to investigate microRNA-195 (miR-195) expression in myocardial ischaemia–reperfusion (I/R) injury and the roles of miR-195 in cardiomyocyte apoptosis though targeting Bcl-2. A mouse model of I/R injury was established. MiR-195 expression levels were detected by real-time quantitative PCR (qPCR), and the cardiomyocyte apoptosis was detected by TUNEL assay. After cardiomyocytes isolated from neonatal rats and transfected with miR-195 mimic or inhibitor, the hypoxia/reoxygenation (H/R) injury model was established. Cardiomyocyte apoptosis and mitochondrial membrane potential were evaluated using flow cytometry. Bcl-2 and Bax mRNA expressions were detected by RT-PCR. Bcl-2, Bax and cytochrome c (Cyt-c) protein levels were determined by Western blot. Caspase-3 and caspase-9 activities were assessed by luciferase assay. Compared with the sham group, miR-195 expression levels and rate of cardiomyocyte apoptosis increased significantly in I/R group (both
P |
| doi_str_mv | 10.1007/s12041-016-0616-3 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_1787973395</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A717820555</galeid><sourcerecordid>A717820555</sourcerecordid><originalsourceid>FETCH-LOGICAL-c482t-374a9d407c21321820bf80acbb3d87e948669d3ade8efa98f1fc8cc5c7d259913</originalsourceid><addsrcrecordid>eNp1kctKxDAUhosoqKMP4K7gxk01l3aSLAfxBqIgug6Z5GTM0DY1aRfd-Q6-oU9iyrgYRQnkdr7_8HP-LDvB6BwjxC4iJqjEBcLzAs3TRneyAyQYLRijeDfdESEFppTuZ4cxrqcnQ-QgM0--htzbvHE6-KeHRYFFlbs21yoY55vR67GHXHW-6310MZXMoMHkyzGfihOl6txF_aqgcerz_SNAB8EO0fk20eshjEfZnlV1hOPvc5a9XF89X94W9483d5eL-0KXnPQFZaUSpkRME0wJ5gQtLUdKL5fUcAai5PO5MFQZ4GCV4BZbzbWuNDOkEgLTWXa26dsF_zZA7GWTjEFdqxb8ECVmnKWZUFEl9PQXuvZDaJO7icKUVyXdolaqBula6_ug9NRULljiCKqqiTr_g0rLpIlo34J16f-HAG8EaeQxBrCyC65RYZQYySlOuYlTpjjlFKekSUM2mpjYdgVhy_C_oi-n86Hy</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1781385435</pqid></control><display><type>article</type><title>Role of microRNA-195 in cardiomyocyte apoptosis induced by myocardial ischaemia–reperfusion injury</title><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Indian Academy of Sciences</source><source>Springer Nature - Complete Springer Journals</source><creator>GAO, CHANG-KUI ; LIU, HUI ; CUI, CHENG-JI ; LIANG, ZHAO-GUANG ; YAO, HONG ; TIAN, YE</creator><creatorcontrib>GAO, CHANG-KUI ; LIU, HUI ; CUI, CHENG-JI ; LIANG, ZHAO-GUANG ; YAO, HONG ; TIAN, YE</creatorcontrib><description>This study aims to investigate microRNA-195 (miR-195) expression in myocardial ischaemia–reperfusion (I/R) injury and the roles of miR-195 in cardiomyocyte apoptosis though targeting Bcl-2. A mouse model of I/R injury was established. MiR-195 expression levels were detected by real-time quantitative PCR (qPCR), and the cardiomyocyte apoptosis was detected by TUNEL assay. After cardiomyocytes isolated from neonatal rats and transfected with miR-195 mimic or inhibitor, the hypoxia/reoxygenation (H/R) injury model was established. Cardiomyocyte apoptosis and mitochondrial membrane potential were evaluated using flow cytometry. Bcl-2 and Bax mRNA expressions were detected by RT-PCR. Bcl-2, Bax and cytochrome c (Cyt-c) protein levels were determined by Western blot. Caspase-3 and caspase-9 activities were assessed by luciferase assay. Compared with the sham group, miR-195 expression levels and rate of cardiomyocyte apoptosis increased significantly in I/R group (both
P
<0.05). Compared to H/R + negative control (NC) group, rate of cardiomyocyte apoptosis increased in H/R + miR-195 mimic group while decreased in H/R + miR-195 inhibitor group (both
P
<0.05). MiR-195 knockdown alleviated the loss of mitochondrial membrane potential (
P
<0.05). MiR-195 overexpression decreased Bcl-2 mRNA and protein expression, increased BaxmRNA and protein expression, Cyt-c protein expression and caspase-3 and caspase-9 activities (all
P
<0.05). While, downregulated MiR-195 increased Bcl-2 mRNA and protein expression, decreased Bax mRNA and protein expression, Cyt-c protein expression and caspase-3 and caspase-9 activities (all
P
<0.05). Our study identified that miR-195 expression was upregulated in myocardial I/R injury, and miR-195 overexpression may promote cardiomyocyte apoptosis by targeting Bcl-2 and inducing mitochondrial apoptotic pathway.</description><identifier>ISSN: 0022-1333</identifier><identifier>EISSN: 0973-7731</identifier><identifier>DOI: 10.1007/s12041-016-0616-3</identifier><language>eng</language><publisher>New Delhi: Springer India</publisher><subject>Analysis ; Animal Genetics and Genomics ; Apoptosis ; Biomedical and Life Sciences ; Cardiomyocytes ; Cardiovascular disease ; Cytochrome c ; Evolutionary Biology ; Ischemia ; Life Sciences ; Microbial Genetics and Genomics ; MicroRNA ; MicroRNAs ; Plant Genetics and Genomics ; Protein expression ; Research Article</subject><ispartof>Journal of genetics, 2016-03, Vol.95 (1), p.99-108</ispartof><rights>Indian Academy of Sciences 2016</rights><rights>COPYRIGHT 2016 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-374a9d407c21321820bf80acbb3d87e948669d3ade8efa98f1fc8cc5c7d259913</citedby><cites>FETCH-LOGICAL-c482t-374a9d407c21321820bf80acbb3d87e948669d3ade8efa98f1fc8cc5c7d259913</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12041-016-0616-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12041-016-0616-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids></links><search><creatorcontrib>GAO, CHANG-KUI</creatorcontrib><creatorcontrib>LIU, HUI</creatorcontrib><creatorcontrib>CUI, CHENG-JI</creatorcontrib><creatorcontrib>LIANG, ZHAO-GUANG</creatorcontrib><creatorcontrib>YAO, HONG</creatorcontrib><creatorcontrib>TIAN, YE</creatorcontrib><title>Role of microRNA-195 in cardiomyocyte apoptosis induced by myocardial ischaemia–reperfusion injury</title><title>Journal of genetics</title><addtitle>J Genet</addtitle><description>This study aims to investigate microRNA-195 (miR-195) expression in myocardial ischaemia–reperfusion (I/R) injury and the roles of miR-195 in cardiomyocyte apoptosis though targeting Bcl-2. A mouse model of I/R injury was established. MiR-195 expression levels were detected by real-time quantitative PCR (qPCR), and the cardiomyocyte apoptosis was detected by TUNEL assay. After cardiomyocytes isolated from neonatal rats and transfected with miR-195 mimic or inhibitor, the hypoxia/reoxygenation (H/R) injury model was established. Cardiomyocyte apoptosis and mitochondrial membrane potential were evaluated using flow cytometry. Bcl-2 and Bax mRNA expressions were detected by RT-PCR. Bcl-2, Bax and cytochrome c (Cyt-c) protein levels were determined by Western blot. Caspase-3 and caspase-9 activities were assessed by luciferase assay. Compared with the sham group, miR-195 expression levels and rate of cardiomyocyte apoptosis increased significantly in I/R group (both
P
<0.05). Compared to H/R + negative control (NC) group, rate of cardiomyocyte apoptosis increased in H/R + miR-195 mimic group while decreased in H/R + miR-195 inhibitor group (both
P
<0.05). MiR-195 knockdown alleviated the loss of mitochondrial membrane potential (
P
<0.05). MiR-195 overexpression decreased Bcl-2 mRNA and protein expression, increased BaxmRNA and protein expression, Cyt-c protein expression and caspase-3 and caspase-9 activities (all
P
<0.05). While, downregulated MiR-195 increased Bcl-2 mRNA and protein expression, decreased Bax mRNA and protein expression, Cyt-c protein expression and caspase-3 and caspase-9 activities (all
P
<0.05). Our study identified that miR-195 expression was upregulated in myocardial I/R injury, and miR-195 overexpression may promote cardiomyocyte apoptosis by targeting Bcl-2 and inducing mitochondrial apoptotic pathway.</description><subject>Analysis</subject><subject>Animal Genetics and Genomics</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiomyocytes</subject><subject>Cardiovascular disease</subject><subject>Cytochrome c</subject><subject>Evolutionary Biology</subject><subject>Ischemia</subject><subject>Life Sciences</subject><subject>Microbial Genetics and Genomics</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>Plant Genetics and Genomics</subject><subject>Protein expression</subject><subject>Research Article</subject><issn>0022-1333</issn><issn>0973-7731</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kctKxDAUhosoqKMP4K7gxk01l3aSLAfxBqIgug6Z5GTM0DY1aRfd-Q6-oU9iyrgYRQnkdr7_8HP-LDvB6BwjxC4iJqjEBcLzAs3TRneyAyQYLRijeDfdESEFppTuZ4cxrqcnQ-QgM0--htzbvHE6-KeHRYFFlbs21yoY55vR67GHXHW-6310MZXMoMHkyzGfihOl6txF_aqgcerz_SNAB8EO0fk20eshjEfZnlV1hOPvc5a9XF89X94W9483d5eL-0KXnPQFZaUSpkRME0wJ5gQtLUdKL5fUcAai5PO5MFQZ4GCV4BZbzbWuNDOkEgLTWXa26dsF_zZA7GWTjEFdqxb8ECVmnKWZUFEl9PQXuvZDaJO7icKUVyXdolaqBula6_ug9NRULljiCKqqiTr_g0rLpIlo34J16f-HAG8EaeQxBrCyC65RYZQYySlOuYlTpjjlFKekSUM2mpjYdgVhy_C_oi-n86Hy</recordid><startdate>20160301</startdate><enddate>20160301</enddate><creator>GAO, CHANG-KUI</creator><creator>LIU, HUI</creator><creator>CUI, CHENG-JI</creator><creator>LIANG, ZHAO-GUANG</creator><creator>YAO, HONG</creator><creator>TIAN, YE</creator><general>Springer India</general><general>Springer</general><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7SS</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>20160301</creationdate><title>Role of microRNA-195 in cardiomyocyte apoptosis induced by myocardial ischaemia–reperfusion injury</title><author>GAO, CHANG-KUI ; LIU, HUI ; CUI, CHENG-JI ; LIANG, ZHAO-GUANG ; YAO, HONG ; TIAN, YE</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-374a9d407c21321820bf80acbb3d87e948669d3ade8efa98f1fc8cc5c7d259913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Analysis</topic><topic>Animal Genetics and Genomics</topic><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Cardiomyocytes</topic><topic>Cardiovascular disease</topic><topic>Cytochrome c</topic><topic>Evolutionary Biology</topic><topic>Ischemia</topic><topic>Life Sciences</topic><topic>Microbial Genetics and Genomics</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>Plant Genetics and Genomics</topic><topic>Protein expression</topic><topic>Research Article</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GAO, CHANG-KUI</creatorcontrib><creatorcontrib>LIU, HUI</creatorcontrib><creatorcontrib>CUI, CHENG-JI</creatorcontrib><creatorcontrib>LIANG, ZHAO-GUANG</creatorcontrib><creatorcontrib>YAO, HONG</creatorcontrib><creatorcontrib>TIAN, YE</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><jtitle>Journal of genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GAO, CHANG-KUI</au><au>LIU, HUI</au><au>CUI, CHENG-JI</au><au>LIANG, ZHAO-GUANG</au><au>YAO, HONG</au><au>TIAN, YE</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of microRNA-195 in cardiomyocyte apoptosis induced by myocardial ischaemia–reperfusion injury</atitle><jtitle>Journal of genetics</jtitle><stitle>J Genet</stitle><date>2016-03-01</date><risdate>2016</risdate><volume>95</volume><issue>1</issue><spage>99</spage><epage>108</epage><pages>99-108</pages><issn>0022-1333</issn><eissn>0973-7731</eissn><abstract>This study aims to investigate microRNA-195 (miR-195) expression in myocardial ischaemia–reperfusion (I/R) injury and the roles of miR-195 in cardiomyocyte apoptosis though targeting Bcl-2. A mouse model of I/R injury was established. MiR-195 expression levels were detected by real-time quantitative PCR (qPCR), and the cardiomyocyte apoptosis was detected by TUNEL assay. After cardiomyocytes isolated from neonatal rats and transfected with miR-195 mimic or inhibitor, the hypoxia/reoxygenation (H/R) injury model was established. Cardiomyocyte apoptosis and mitochondrial membrane potential were evaluated using flow cytometry. Bcl-2 and Bax mRNA expressions were detected by RT-PCR. Bcl-2, Bax and cytochrome c (Cyt-c) protein levels were determined by Western blot. Caspase-3 and caspase-9 activities were assessed by luciferase assay. Compared with the sham group, miR-195 expression levels and rate of cardiomyocyte apoptosis increased significantly in I/R group (both
P
<0.05). Compared to H/R + negative control (NC) group, rate of cardiomyocyte apoptosis increased in H/R + miR-195 mimic group while decreased in H/R + miR-195 inhibitor group (both
P
<0.05). MiR-195 knockdown alleviated the loss of mitochondrial membrane potential (
P
<0.05). MiR-195 overexpression decreased Bcl-2 mRNA and protein expression, increased BaxmRNA and protein expression, Cyt-c protein expression and caspase-3 and caspase-9 activities (all
P
<0.05). While, downregulated MiR-195 increased Bcl-2 mRNA and protein expression, decreased Bax mRNA and protein expression, Cyt-c protein expression and caspase-3 and caspase-9 activities (all
P
<0.05). Our study identified that miR-195 expression was upregulated in myocardial I/R injury, and miR-195 overexpression may promote cardiomyocyte apoptosis by targeting Bcl-2 and inducing mitochondrial apoptotic pathway.</abstract><cop>New Delhi</cop><pub>Springer India</pub><doi>10.1007/s12041-016-0616-3</doi><tpages>10</tpages></addata></record> |
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| source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Indian Academy of Sciences; Springer Nature - Complete Springer Journals |
| subjects | Analysis Animal Genetics and Genomics Apoptosis Biomedical and Life Sciences Cardiomyocytes Cardiovascular disease Cytochrome c Evolutionary Biology Ischemia Life Sciences Microbial Genetics and Genomics MicroRNA MicroRNAs Plant Genetics and Genomics Protein expression Research Article |
| title | Role of microRNA-195 in cardiomyocyte apoptosis induced by myocardial ischaemia–reperfusion injury |
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