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MicroRNA-138 plays a role in hypoxic pulmonary vascular remodelling by targeting Mst1

Shanshan Li1, Yajuan Ran, Dandan Zhang

  • 1Department of Biopharmaceutical Sciences, College of Pharmacy, Harbin Medical University, Daqing, Heilongjiang 163319, China.

The Biochemical Journal
|March 15, 2013
PubMed

Insights

MicroRNA-138 (miR-138) suppresses apoptosis in pulmonary artery smooth muscle cells, offering a potential therapeutic target for pulmonary arterial hypertension and hypoxic pulmonary vascular remodeling.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Cell Biology

Background:

  • Unbalanced apoptosis contributes to vascular remodeling in pulmonary arterial hypertension (PAH), but underlying mechanisms remain unclear.
  • MicroRNAs (miRNAs) are key regulators of cell fate, including apoptosis, and may influence PAH development.

Purpose of the Study:

  • To investigate the role of specific miRNAs in regulating apoptosis of pulmonary artery smooth muscle cells (PASMCs).
  • To identify potential miRNA targets and pathways involved in hypoxic pulmonary vascular remodeling (HPVR).

Main Methods:

  • Studied the effect of various miRNAs on cultured PASMC apoptosis.
  • Investigated the expression and regulation of miR-138 under hypoxic conditions.
  • Analyzed the impact of exogenous miR-138 on apoptosis, caspase activation, and Bcl-2 signaling.
  • Identified Mst1 as a potential miR-138 target and assessed the role of the Akt pathway.

Main Results:

  • miR-138 is expressed in PASMCs and regulated by hypoxia.
  • Exogenous miR-138 suppressed PASMC apoptosis, caspase activation, and altered Bcl-2 signaling.
  • miR-138 targets the apoptosis-amplifying kinase Mst1.
  • The anti-apoptotic effect of miR-138 is dependent on Akt pathway activation.

Conclusions:

  • miR-138 acts as a negative regulator of PASMC apoptosis.
  • miR-138 plays a significant role in HPVR and may be a therapeutic target for PAH.

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