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Regulation and function of miR-214 in pulmonary arterial hypertension

Hannah C Stevens1, Lin Deng1, Jennifer S Grant2

  • 1Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom; Present affiliation: Queens Medical Research Institute, University of Edinburgh, Edinburgh.

Pulmonary Circulation
|May 11, 2016
PubMed

Insights

MicroRNA-214 dysregulation contributes to pulmonary arterial hypertension (PAH) complications. Loss of miR-214 exacerbates right ventricular hypertrophy, potentially worsening heart failure in PAH patients.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Pulmonary Hypertension Research

Background:

  • MicroRNA (miRNA) dysregulation is implicated in disease pathogenesis, including pulmonary arterial hypertension (PAH).
  • Specific miRNAs, such as the miR-214 stem loop and miR-199a family, are investigated for their roles in PAH.
  • PAH is characterized by increased pulmonary vascular resistance and right ventricular (RV) dysfunction.

Purpose of the Study:

  • To investigate the role of the miR-214 stem loop and miR-199a miRNAs in the context of pulmonary arterial hypertension (PAH).
  • To determine the effect of miR-214 deficiency on the development of PAH-associated right ventricular hypertrophy (RVH).

Main Methods:

  • Utilized the Sugen (SU) 5416 hypoxia model in mice and rats to induce PAH.
  • Assessed miRNA expression in lung and right ventricle tissues.
  • Examined miR-214 knockout (miR-214(-/-)) mice under normoxic and hypoxic conditions.
  • Measured right ventricular systolic pressure, remodeling, and hypertrophy.
  • Validated miR-214 targets, including phosphatase and tensin homolog (PTEN).

Main Results:

  • Four specific miRNAs, including miR-214, were upregulated in the lungs and RV of PAH model animals.
  • miRNA expression increased in pulmonary artery smooth muscle cells treated with TGF-β1.
  • miR-214(-/-) mice showed no significant changes in RV systolic pressure or remodeling compared to wild-type controls.
  • However, hypoxic miR-214(-/-) male mice exhibited significantly increased RV hypertrophy.
  • The validated miR-214 target, PTEN, was found to be upregulated in miR-214(-/-) mice.

Conclusions:

  • Loss of miR-214 leads to increased right ventricular hypertrophy in a model of pulmonary arterial hypertension.
  • Upregulation of PTEN in miR-214 deficient mice may contribute to RVH.
  • miR-214 deficiency may play a role in the progression of heart failure associated with PAH.
Keywords:
Sugen 5416 hypoxia modelmicroRNA-199right ventricular hypertrophytransforming growth factor β1

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