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P53 Promotes Retinoid Acid-induced Smooth Muscle Cell Differentiation by Targeting Myocardin

Zhou Tan1, Jingya Li1, Xuejing Zhang2

  • 11 Key Laboratory of Organ Development and Regeneration of Zhejiang Province, Institute of Life Sciences, College of Life Sciences, Hangzhou Normal University , Hangzhou, China .

Stem Cells and Development
|February 28, 2018
PubMed

Insights

The tumor suppressor gene TP53 regulates smooth muscle cell (SMC) differentiation by targeting Myocardin. This finding offers potential new therapeutic targets for vascular diseases.

Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Cardiovascular Research

Background:

  • The tumor suppressor gene TP53 is crucial for cellular functions, but its role in smooth muscle cell (SMC) differentiation from embryonic stem cells (ESCs) is largely unknown.
  • SMC differentiation is vital for vascular development, blood pressure regulation, and understanding vascular diseases like atherosclerosis and hypertension.

Purpose of the Study:

  • To investigate the functional role of p53 in embryonic stem cell-derived smooth muscle cell differentiation.
  • To elucidate the molecular mechanisms by which p53 influences SMC differentiation and its potential implications in vascular diseases.

Main Methods:

  • Utilized retinoid acid (RA)-induced in vitro differentiation models of mouse ESCs into SMCs.
  • Employed shRNA to suppress p53 expression and assessed its impact on SMC differentiation.
  • Investigated the p53-Myocardin interaction using bioinformatic analysis, luciferase reporter assays, and chromatin immunoprecipitation.
  • Examined the in vivo effects of SMC-selective p53 overexpression on injury-induced neointimal formation.

Main Results:

  • p53 expression increased during RA-induced in vitro differentiation of ESCs into SMCs.
  • Suppression of p53 significantly reduced RA-induced SMC differentiation.
  • Identified Myocardin as a direct transcriptional target of p53.
  • SMC-selective p53 overexpression inhibited injury-induced neointimal formation in vivo.

Conclusions:

  • p53 plays a significant regulatory role in SMC differentiation, partly through its target gene Myocardin.
  • These findings highlight p53 and Myocardin as key players in SMC biology and suggest potential therapeutic targets for vascular diseases.
Keywords:
Myocardindifferentiationembryonic stem cellsp53retinoic acidsmooth muscle cells

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