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Coronary artery disease associated gene Phactr1 modulates severity of vascular calcification in vitro

Redouane Aherrahrou1, Zouhair Aherrahrou2, Heribert Schunkert3

  • 1Institute for Cardiogenetics, University of Lübeck, DZHK (German Research Centre for Cardiovascular Research), Partner Site Hamburg/Lübeck/Kie, University Heart Center Luebeck, 23562 Lübeck, Germany; Center for Public Health Genomics, Department of Biomedical Engineering, University of Virginia, Charlottesville, VA, USA.

Biochemical and Biophysical Research Communications
|July 20, 2017
PubMed

Insights

The phosphatase and actin regulator 1 (PHACTR1) gene influences vascular calcification. Lowering PHACTR1 levels in smooth muscle cells reduces calcification, while increasing them enhances it, revealing a key mechanism in atherosclerosis.

Area of Science:

  • Cardiovascular Biology
  • Molecular Genetics
  • Vascular Biology

Background:

  • Vascular calcification is a hallmark of atherosclerosis, strongly linked to coronary artery disease (CAD) and myocardial infarction (MI).
  • Genome-wide association studies (GWAS) have identified several genes contributing to CAD/MI and coronary artery calcification (CAC), but their functional roles remain unclear.
  • PHACTR1 is one such identified risk gene, but its specific contribution to vascular calcification mechanisms requires elucidation.

Purpose of the Study:

  • To investigate the functional role of Phosphatase and Actin Regulator 1 (PHACTR1) in regulating vascular calcification.
  • To determine if PHACTR1 expression levels modulate the extent of calcification in smooth muscle cells (SMCs).

Main Methods:

  • Murine embryonic stem cells (mESCs) were engineered for stable up- or down-regulation of Phactr1.
  • mESCs were differentiated into SMCs and subjected to osteogenic conditions to induce calcification.
  • Calcium phosphate deposition was quantified, and gene expression of Phactr1 and the osteogenic marker osteopontin was analyzed using RT-PCR.

Main Results:

  • Gene expression of Phactr1 positively correlated with the degree of calcification in both mESC-derived SMCs and primary human aortic SMCs.
  • Down-regulation of Phactr1 significantly decreased calcification and reduced osteopontin expression.
  • Overexpression of Phactr1 in mESC-derived SMCs led to enhanced mineralization.

Conclusions:

  • PHACTR1 expression increases with the progression of vascular calcification.
  • Modulating PHACTR1 levels in SMCs directly impacts the severity of vascular calcification.
  • PHACTR1 is a key regulator of vascular calcification, offering potential therapeutic targets for atherosclerosis-related diseases.

Keywords:
PHACTR1Smooth muscle cellsVascular calcification

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