CDK6 mediates the effect of attenuation of miR-1 on provoking cardiomyocyte hypertrophy
MicroRNA-1 (miR-1) is approved involved in cardiac hypertrophy, but the underlying molecular mechanisms of miR-1 in cardiac hypertrophy are not well elucidated. The present study aimed to investigate the potential role of miR-1 in modulating CDKs-Rb pathway during cardiomyocyte hypertrophy. A rat mo...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2016-01, Vol.412 (1-2), p.289-296 |
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| creator | Yuan, Weiwei Tang, Chunmei Zhu, Wensi Zhu, Jiening Lin, Qiuxiong Fu, Yongheng Deng, Chunyu Xue, Yumei Yang, Min Wu, Shulin Shan, Zhixin |
| description | MicroRNA-1 (miR-1) is approved involved in cardiac hypertrophy, but the underlying molecular mechanisms of miR-1 in cardiac hypertrophy are not well elucidated. The present study aimed to investigate the potential role of miR-1 in modulating CDKs-Rb pathway during cardiomyocyte hypertrophy. A rat model of hypertrophy was established with abdominal aortic constriction, and a cell model of hypertrophy was also achieved based on PE-promoted neonatal rat ventricular cardiomyocytes (NRVCs). We demonstrated that miR-1 expression was markedly decreased in hypertrophic myocardium and hypertrophic cardiomyocytes. Dual luciferase reporter assays revealed that miR-1 interacted with the 3′UTR of CDK6, and miR-1 was verified to inhibit CDK6 expression at the posttranscriptional level. CDK6 protein expression was observed increased in hypertrophic myocardium and hypertrophic cardiomyocytes. Morover, miR-1 mimic, in parallel to CDK6 siRNA, could inhibit PE-induced hypertrophy of NRVCs, with decreases in cell size, newly transcribed RNA, expressions of ANF and
β
-MHC, and the phosphorylated pRb. Taken together, our results reveal that derepression of CDK6 and activation of Rb pathway contributes to the effect of attenuation of miR-1 on provoking cardiomyocyte hypertrophy. |
| doi_str_mv | 10.1007/s11010-015-2635-4 |
| format | Article |
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β
-MHC, and the phosphorylated pRb. Taken together, our results reveal that derepression of CDK6 and activation of Rb pathway contributes to the effect of attenuation of miR-1 on provoking cardiomyocyte hypertrophy.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-015-2635-4</identifier><identifier>PMID: 26699910</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Biochemistry ; Biomedical and Life Sciences ; Cardiology ; Cardiomegaly - metabolism ; Cardiomyocytes ; Cellular biology ; Cyclin-Dependent Kinase 6 - genetics ; Cyclin-Dependent Kinase 6 - physiology ; Down-Regulation ; Heart ; Heart hypertrophy ; Life Sciences ; Luciferase ; Male ; Medical Biochemistry ; MicroRNA ; MicroRNAs ; MicroRNAs - metabolism ; Myocytes, Cardiac - pathology ; Oncology ; Protein expression ; Rats ; Rats, Sprague-Dawley ; RNA, Small Interfering - genetics ; Signal transduction</subject><ispartof>Molecular and cellular biochemistry, 2016-01, Vol.412 (1-2), p.289-296</ispartof><rights>Springer Science+Business Media New York 2015</rights><rights>COPYRIGHT 2016 Springer</rights><rights>Springer Science+Business Media New York 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c509t-f34908b25b1fa7b81fe1d2c7ba5ddb7733e47de4d1ec01cefb8c73a52c57bfd63</citedby><cites>FETCH-LOGICAL-c509t-f34908b25b1fa7b81fe1d2c7ba5ddb7733e47de4d1ec01cefb8c73a52c57bfd63</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/s11010-015-2635-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-015-2635-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26699910$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yuan, Weiwei</creatorcontrib><creatorcontrib>Tang, Chunmei</creatorcontrib><creatorcontrib>Zhu, Wensi</creatorcontrib><creatorcontrib>Zhu, Jiening</creatorcontrib><creatorcontrib>Lin, Qiuxiong</creatorcontrib><creatorcontrib>Fu, Yongheng</creatorcontrib><creatorcontrib>Deng, Chunyu</creatorcontrib><creatorcontrib>Xue, Yumei</creatorcontrib><creatorcontrib>Yang, Min</creatorcontrib><creatorcontrib>Wu, Shulin</creatorcontrib><creatorcontrib>Shan, Zhixin</creatorcontrib><title>CDK6 mediates the effect of attenuation of miR-1 on provoking cardiomyocyte hypertrophy</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>MicroRNA-1 (miR-1) is approved involved in cardiac hypertrophy, but the underlying molecular mechanisms of miR-1 in cardiac hypertrophy are not well elucidated. The present study aimed to investigate the potential role of miR-1 in modulating CDKs-Rb pathway during cardiomyocyte hypertrophy. A rat model of hypertrophy was established with abdominal aortic constriction, and a cell model of hypertrophy was also achieved based on PE-promoted neonatal rat ventricular cardiomyocytes (NRVCs). We demonstrated that miR-1 expression was markedly decreased in hypertrophic myocardium and hypertrophic cardiomyocytes. Dual luciferase reporter assays revealed that miR-1 interacted with the 3′UTR of CDK6, and miR-1 was verified to inhibit CDK6 expression at the posttranscriptional level. CDK6 protein expression was observed increased in hypertrophic myocardium and hypertrophic cardiomyocytes. Morover, miR-1 mimic, in parallel to CDK6 siRNA, could inhibit PE-induced hypertrophy of NRVCs, with decreases in cell size, newly transcribed RNA, expressions of ANF and
β
-MHC, and the phosphorylated pRb. Taken together, our results reveal that derepression of CDK6 and activation of Rb pathway contributes to the effect of attenuation of miR-1 on provoking cardiomyocyte hypertrophy.</description><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiology</subject><subject>Cardiomegaly - metabolism</subject><subject>Cardiomyocytes</subject><subject>Cellular biology</subject><subject>Cyclin-Dependent Kinase 6 - genetics</subject><subject>Cyclin-Dependent Kinase 6 - physiology</subject><subject>Down-Regulation</subject><subject>Heart</subject><subject>Heart hypertrophy</subject><subject>Life Sciences</subject><subject>Luciferase</subject><subject>Male</subject><subject>Medical Biochemistry</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Oncology</subject><subject>Protein expression</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>RNA, Small Interfering - 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Academic</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yuan, Weiwei</au><au>Tang, Chunmei</au><au>Zhu, Wensi</au><au>Zhu, Jiening</au><au>Lin, Qiuxiong</au><au>Fu, Yongheng</au><au>Deng, Chunyu</au><au>Xue, Yumei</au><au>Yang, Min</au><au>Wu, Shulin</au><au>Shan, Zhixin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CDK6 mediates the effect of attenuation of miR-1 on provoking cardiomyocyte hypertrophy</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2016-01-01</date><risdate>2016</risdate><volume>412</volume><issue>1-2</issue><spage>289</spage><epage>296</epage><pages>289-296</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>MicroRNA-1 (miR-1) is approved involved in cardiac hypertrophy, but the underlying molecular mechanisms of miR-1 in cardiac hypertrophy are not well elucidated. The present study aimed to investigate the potential role of miR-1 in modulating CDKs-Rb pathway during cardiomyocyte hypertrophy. A rat model of hypertrophy was established with abdominal aortic constriction, and a cell model of hypertrophy was also achieved based on PE-promoted neonatal rat ventricular cardiomyocytes (NRVCs). We demonstrated that miR-1 expression was markedly decreased in hypertrophic myocardium and hypertrophic cardiomyocytes. Dual luciferase reporter assays revealed that miR-1 interacted with the 3′UTR of CDK6, and miR-1 was verified to inhibit CDK6 expression at the posttranscriptional level. CDK6 protein expression was observed increased in hypertrophic myocardium and hypertrophic cardiomyocytes. Morover, miR-1 mimic, in parallel to CDK6 siRNA, could inhibit PE-induced hypertrophy of NRVCs, with decreases in cell size, newly transcribed RNA, expressions of ANF and
β
-MHC, and the phosphorylated pRb. Taken together, our results reveal that derepression of CDK6 and activation of Rb pathway contributes to the effect of attenuation of miR-1 on provoking cardiomyocyte hypertrophy.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>26699910</pmid><doi>10.1007/s11010-015-2635-4</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Biochemistry Biomedical and Life Sciences Cardiology Cardiomegaly - metabolism Cardiomyocytes Cellular biology Cyclin-Dependent Kinase 6 - genetics Cyclin-Dependent Kinase 6 - physiology Down-Regulation Heart Heart hypertrophy Life Sciences Luciferase Male Medical Biochemistry MicroRNA MicroRNAs MicroRNAs - metabolism Myocytes, Cardiac - pathology Oncology Protein expression Rats Rats, Sprague-Dawley RNA, Small Interfering - genetics Signal transduction |
| title | CDK6 mediates the effect of attenuation of miR-1 on provoking cardiomyocyte hypertrophy |
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