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miR-199-sponge transgenic mice develop physiological cardiac hypertrophy.

Zhenhua Li1, Lantao Liu1, Ning Hou1

  • 1State Key Laboratory of Proteomics, Genetic Laboratory of Development and Disease, Institute of Biotechnology, 20 Dongdajie, Beijing 100071, China.

Cardiovascular Research
|March 16, 2016
PubMed
Summary

Endogenous miR-199 normally prevents physiological cardiac hypertrophy. Inhibiting miR-199 in mice unexpectedly led to beneficial cardiac growth, revealing its role in maintaining heart homeostasis.

Keywords:
Physiological cardiac hypertrophyTransgenic micemiR-199 familymiRNA sponge

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Gene Regulation

Background:

  • The miR-199 family, including miR-199a-5p and miR-199b-5p, is known to promote pathological cardiac hypertrophy when overexpressed.
  • The role of endogenous miR-199 in normal cardiac development and homeostasis remains largely uncharacterized.

Purpose of the Study:

  • To investigate the physiological function of the endogenous miR-199 family in maintaining cardiac homeostasis.
  • To elucidate the role of endogenous miR-199 in cardiac development and disease processes.

Main Methods:

  • Generation of a sponge transgenic mouse model with specific disruption of miR-199 in the heart.
  • Analysis of cardiac morphology, heart weight, cardiomyocyte size, and cardiac function in the modified mice.
  • Identification of target genes regulated by the miR-199 family.

Main Results:

  • Knockdown of endogenous miR-199 resulted in physiological cardiac hypertrophy, evidenced by increased heart weight and cardiomyocyte size.
  • Cardiac morphology and function remained normal despite the hypertrophy.
  • PGC1α was identified as a direct target gene of the miR-199 family and was found to be upregulated in the miR-199 disrupted mice.

Conclusions:

  • Inhibition of endogenous miR-199 leads to physiological cardiac hypertrophy, likely mediated by the upregulation of PGC1α.
  • This study uncovers a novel, protective role for endogenous miR-199 in maintaining cardiac homeostasis.
  • Endogenous miR-199 acts as a crucial regulator in preventing excessive cardiac growth.