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MEF2 C 介导 microRNA-214发挥抑制心肌细胞肥大的作用

唐春梅 吴书林 单志新 朱杰宁 朱文思 林秋雄 胡志琴 符永恒 张梦珍 邓春玉 谭虹虹

中国病理生理杂志2016,Vol.32Issue(8):1345-1350,6.
中国病理生理杂志2016,Vol.32Issue(8):1345-1350,6.DOI:10.3969/j.issn.1000-4718.2016.08.001

MEF2 C 介导 microRNA-214发挥抑制心肌细胞肥大的作用

MEF2C mediates inhibitory effect of microRNA-214 on cardiomyocyte hypertrophy

唐春梅 1吴书林 2单志新 3朱杰宁 3朱文思 3林秋雄 1胡志琴 2符永恒 3张梦珍 1邓春玉 2谭虹虹3

作者信息

  • 1. 南方医科大学,广东广州510515
  • 2. 广东省心血管病研究所,广东省人民医院,广东省医学科学院,广东广州510080
  • 3. 广东省心血管病研究所,广东省人民医院,广东省医学科学院,广东广州510080
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摘要

Abstract

AIM:To investigate the effect of microRNA-214 ( miR-214) on cardiomyocyte hypertrophy and the expression of the potential target genes .METHODS:A cell model of hypertrophy was established based on angiotensin-Ⅱ( Ang-Ⅱ)-induced neonatal mouse ventricular cardiomyocytes ( NMVCs) .Dual luciferase reporter assay was performed to verify the interaction between miR-214 and the 3’ UTR of MEF2C.The expression of MEF2C and hypertrophy-related genes at mRNA and protein levels was determined by RT-qPCR and Western blot , respectively .RESULTS:The expression of ANP, ACTA1,β-MHC and miR-214 was markedly increased in Ang-Ⅱ-induced hypertrophic cardiomyocytes .Dual lu-ciferase reporter assay revealed that miR-214 interacted with the 3’ UTR of MEF2C, and miR-214 was verified to inhibit MEF2C expression at the transcriptional level .The protein expression of MEF2C was markedly increased in the hypertro-phic cardiomyocytes .Moreover, miR-214 mimic, in parallel to MEF2C siRNA, inhibited the expression of hypertrophy-re-lated genes in Ang-Ⅱ-induced NMVCs.CONCLUSION:MEF2C is a target gene of miR-214, which mediates the effect of miR-214 on attenuating cardiomyocyte hypertrophy .

关键词

心肌肥厚/微小RNA-214/MEF2C/心肌细胞

Key words

Cardiac hypertrophy/MicroRNA-214/MEF2C/Cardiomyocytes

分类

医药卫生

引用本文复制引用

唐春梅,吴书林,单志新,朱杰宁,朱文思,林秋雄,胡志琴,符永恒,张梦珍,邓春玉,谭虹虹..MEF2 C 介导 microRNA-214发挥抑制心肌细胞肥大的作用[J].中国病理生理杂志,2016,32(8):1345-1350,6.

基金项目

国家自然科学基金资助项目( No.81270222;No.81470439);广东省自然科学基金资助项目( No.2014A030313635);广东省医学研究基金资助项目 ()

中国病理生理杂志

OA北大核心CSCDCSTPCD

1000-4718

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