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Micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s (mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s), the endogenous small non\u2010coding <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s, were recognized to play significant roles in cardiac hypertrophy. But, it remains unknown whether cyclin\/Rb pathway is modulated by mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s during cardiac hypertrophy. This study investigates the potential role of micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\u201016 (miR\u201016) in modulating cyclin\/Rb pathway during cardiomyocyte hypertrophy. An animal model of hypertrophy was established in a rat with abdominal aortic constriction (<jats:styled-content style=\"fixed-case\">AAC<\/jats:styled-content>), and in a mouse with transverse aortic constriction (<jats:styled-content style=\"fixed-case\">TAC<\/jats:styled-content>) and in a mouse with subcutaneous injection of phenylephrine (<jats:styled-content style=\"fixed-case\">PE<\/jats:styled-content>) respectively. In addition, a cell model of hypertrophy was also achieved based on <jats:styled-content style=\"fixed-case\">PE<\/jats:styled-content>\u2010promoted neonatal rat ventricular cardiomyocyte and based on Ang\u2010II\u2010induced neonatal mouse ventricular cardiomyocyte respectively. We demonstrated that miR\u201016 expression was markedly decreased in hypertrophic myocardium and hypertrophic cardiomyocytes in rats and mice. Overexpression of miR\u201016 suppressed rat cardiac hypertrophy and hypertrophic phenotype of cultured cardiomyocytes, and inhibition of miR\u201016 induced a hypertrophic phenotype in cardiomyocytes. Expressions of cyclins D1, D2 and E1, and the phosphorylated pRb were increased in hypertrophic myocardium and hypertrophic cardiomyocytes, but could be reversed by enforced expression of miR\u201016. Cyclins D1, D2 and E1, not pRb, were further validated to be modulated post\u2010transcriptionally by miR\u201016. In addition, the signal transducer and activator of transcription\u20103 and c\u2010Myc were activated during myocardial hypertrophy, and inhibitions of them prevented miR\u201016 attenuation. Therefore, attenuation of miR\u201016 provoke cardiomyocyte hypertrophy <jats:italic>via<\/jats:italic> derepressing the cyclins D1, D2 and E1, and activating cyclin\/Rb pathway, revealing that miR\u201016 might be a target to manage cardiac hypertrophy.<\/jats:p>","DOI":"10.1111\/jcmm.12445","type":"journal-article","created":{"date-parts":[[2015,1,13]],"date-time":"2015-01-13T12:05:09Z","timestamp":1421150709000},"page":"608-619","source":"Crossref","is-referenced-by-count":37,"title":["Attenuation of micro<scp>RNA<\/scp>\u201016 derepresses the cyclins D1, D2 and E1 to provoke cardiomyocyte hypertrophy"],"prefix":"10.1111","volume":"19","author":[{"given":"Shuai","family":"Huang","sequence":"first","affiliation":[{"name":"Medical Research Department of Guangdong General Hospital Guangdong Provincial Cardiovascular Institute Guangdong Academy of Medical Sciences Guangzhou 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