4.6 Article

MicroRNA-29a-3p attenuates ET-1-induced hypertrophic responses in H9c2 cardiomyocytes

Journal

GENE
Volume 585, Issue 1, Pages 44-50

Publisher

ELSEVIER SCIENCE BV
DOI: 10.1016/j.gene.2016.03.015

Keywords

Cardiomyocyte hypertrophy; miR-29a-3p; NFATc4

Funding

  1. National Natural Science Foundation of China [31171303, 31070694, 31270837]
  2. Program for Changjiang Scholars and Innovative Research Team in University of Ministry of Education of China [IRT1166]
  3. Research Fund for the Doctoral Program of Higher Education of China [20111208110001]

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Transcription factor nuclear factor of activated T cells c4 (NFATc4) is the best-characterized target for the development of cardiac hypertrophy. Aberrant microRNA-29 (miR-29) expression is involved in the development of cardiac fibrosis and congestive heart failure. However, whether miR-29 regulates hypertrophic processes is still not clear. In this study, we investigated the potential functions of miR-29a-3p in endothelin-1 (ET-1)-induced cardiomyocyte hypertrophy. We showed that miR-29a-3p was down-regulated in ET-1-treated H9c2 cardiomyocytes. Overexpression of miR-29a-3p significantly reduced ET-1-induced hypertrophic responses in H9c2 cardiomyocytes, which was accompanied by a decrease in NFATc4 expression. miR-29a-3p targeted directly to the 3'-UTR of NFATc4 mRNA and silenced NFATc4 expression. Our results indicate that miR-29a-3p inhibits ET-1-induced cardiomyocyte hypertrophy via inhibiting NFATc4 expression. (C) 2016 Published by Elsevier B.V.

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