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Smooth muscle calponin: an unconventional CArG-dependent gene that antagonizes neointimal formation

Xiaochun Long1, Orazio J Slivano, Sarah L Cowan

  • 1Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, NY 14642, USA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|August 6, 2011
PubMed
Abstract

Insights

A single intronic CArG element is crucial for smooth muscle calponin (CNN1) gene expression in vivo. Overexpressing CNN1 effectively prevents artery remodeling after injury.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Gene Regulation

Background:

  • Smooth muscle calponin (CNN1) gene regulation involves intronic CArG elements.
  • These elements bind serum response factor and show enhancer activity in vitro.
  • Understanding CNN1's role in vascular remodeling is critical.

Purpose of the Study:

  • To assess the in vivo activity of CNN1 intronic CArG elements in transgenic mice.
  • To determine the impact of human CNN1 on injury-induced vascular remodeling.
  • To identify regulatory elements controlling CNN1 expression.

Main Methods:

  • Transgenic mouse models with lacZ reporters and human CNN1 BAC constructs.
  • BAC recombineering to mutate CArG elements.
  • Immunohistochemistry and Western blotting for protein expression analysis.
  • Assessment of neointimal formation and vascular remodeling after arterial injury.

Main Results:

  • Intronic CArG elements were not sufficient for SMC-restricted activity with a lacZ reporter.
  • Deletion of orthologous sequences impaired endogenous Cnn1 promoter activity.
  • A single intronic CArG element was essential for SMC-restricted human CNN1 expression from a BAC.
  • Human CNN1 overexpression suppressed neointimal formation post-injury.
  • Mutations in CArG elements led to outward remodeling and neointimal formation.

Conclusions:

  • A single intronic CArG element is necessary but not sufficient for proper in vivo CNN1 expression.
  • CNN1 overexpression acts as an antagonist to arterial injury-induced neointimal formation.

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