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MicroRNA-134-5p Regulates Media Degeneration through Inhibiting VSMC Phenotypic Switch and Migration in Thoracic

Ying Wang1, Chang-Qing Dong1, Guang-Yin Peng1

  • 1Department of Cardiovascular Surgery of the First Affiliated Hospital & Institute for Cardiovascular Science, Soochow University, Suzhou, Jiangsu, China.

Molecular Therapy. Nucleic Acids
|April 6, 2019
PubMed

Insights

MicroRNA-134-5p is downregulated in thoracic aortic dissection (TAD). Restoring miR-134-5p promotes vascular smooth muscle cell (VSMC) differentiation and inhibits TAD progression by targeting STAT5B/ITGB1.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Genetics and Genomics

Background:

  • Vascular smooth muscle cell (VSMC) dysfunction drives thoracic aortic dissection (TAD).
  • MicroRNAs (miRNAs) play crucial roles in regulating cellular processes relevant to TAD pathogenesis.

Purpose of the Study:

  • To investigate the role of miR-134-5p in human VSMC function and its involvement in TAD development.
  • To identify downstream targets of miR-134-5p in the context of VSMC biology and TAD.

Main Methods:

  • miRNA microarray and qPCR to assess miR-134-5p expression in TAD tissues and human VSMCs.
  • Gain-of-function studies using ectopic miR-134-5p expression to evaluate effects on VSMC differentiation and migration.
  • Identification and validation of STAT5B and ITGB1 as direct targets of miR-134-5p.
  • In vivo studies using an Ang II-induced TAD mouse model treated with Ad-miR-134-5p.

Main Results:

  • miR-134-5p was significantly downregulated in TAD tissues and human VSMCs.
  • Ectopic miR-134-5p expression promoted VSMC differentiation and contractile marker expression (α-SMA, SM22α, MYH11).
  • miR-134-5p inhibited PDGF-BB-induced VSMC phenotypic switch and migration, targeting STAT5B and ITGB1.
  • In vivo administration of Ad-miR-134-5p suppressed aorta dilatation and vascular media degeneration in a mouse model of TAD.

Conclusions:

  • miR-134-5p acts as a novel regulator of vascular remodeling and TAD progression.
  • The miR-134-5p/STAT5B/ITGB1 axis is critical for VSMC function and TAD pathogenesis.
  • Targeting miR-134-5p or its downstream effectors offers potential therapeutic strategies for TAD.
Keywords:
VSMCmedia degenerationmiR-134-5pphenotypic switchthoracic aortic dissection

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