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Updated: Jan 26, 2026

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MicroRNA-126 affects cell apoptosis, proliferation, cell cycle and modulates VEGF/TGF-β levels in pulmonary artery

Y Yuan1, C Shen, S-L Zhao

  • 1Department of Cardiovascular Surgery, Daping Hospital, Army Medical University, Chongqing, China. zhongqianjin@hainan.net.

European Review for Medical and Pharmacological Sciences
|April 20, 2019
PubMed
Abstract

Insights

MicroRNA-126 (miR-126) plays a critical role in pulmonary arterial hypertension (PAH) by influencing endothelial cell apoptosis and proliferation. This study reveals miR-126

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Cell Biology

Background:

  • Pulmonary arterial hypertension (PAH) presents limited therapeutic options, necessitating research into novel treatment strategies.
  • Understanding the molecular mechanisms underlying PAH pathogenesis is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the role of microRNA-126 (miR-126) in the pathogenesis of pulmonary arterial hypertension (PAH).
  • To evaluate the impact of miR-126 on associated signaling pathways and specific mechanisms in PAH.

Main Methods:

  • Pulmonary artery endothelial cells (PAECs) were isolated and treated with miR-126 mimic or inhibitor via viral vectors.
  • Gene expression (SPRED1, PIK3R2, miR-126) was quantified using RT-PCR.
  • Cell apoptosis, proliferation, cell cycle, and levels of VEGF, TGF-β1, and TGF-β3 were assessed using flow cytometry and ELISA.

Main Results:

  • miR-126 overexpression inhibited PAEC apoptosis and promoted proliferation and S-phase cell cycle progression.
  • miR-126 mimic significantly increased VEGF, TGF-β1, and TGF-β3 levels in PAECs.
  • miR-126 expression was inversely correlated with SPRED1 and PIK3R2 in PAECs.

Conclusions:

  • miR-126 significantly influences PAEC apoptosis, proliferation, and cell cycle.
  • miR-126 modulates key signaling molecules including VEGF and TGF-β, suggesting a role in PAH development.
  • Targeting miR-126 may represent a novel therapeutic strategy for pulmonary arterial hypertension.

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