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Updated: Apr 6, 2026

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
08:43

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

Published on: May 31, 2016

20.7K

PDGFRβ signalling regulates local inflammation and synergizes with hypercholesterolaemia to promote atherosclerosis

Chaoyong He1, Shayna C Medley2, Taishan Hu3

  • 1Immunobiology and Cancer Research Program, Oklahoma Medical Research Foundation, 825 North East 13th Street, Oklahoma City, Oklahoma 73013, USA.

Nature Communications
|July 18, 2015
PubMed

Insights

Activating platelet-derived growth factor receptor beta (PDGFRβ) signaling in vascular smooth muscle cells accelerates atherosclerosis. Blocking STAT1 in these cells reduces arterial inflammation and plaque development, highlighting PDGFRβ

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Platelet-derived growth factor (PDGF) influences vascular smooth muscle cells (VSMCs).
  • The specific role of PDGF receptor beta (PDGFRβ) activation in atherosclerosis remains unclear.
  • VSMCs are key players in vascular diseases.

Purpose of the Study:

  • To investigate the direct impact of PDGFRβ activation on VSMCs in atherosclerosis.
  • To elucidate the mechanisms by which PDGFRβ signaling affects arterial inflammation and plaque formation.
  • To assess the therapeutic potential of targeting PDGFRβ-STAT1 signaling in vascular disease.

Main Methods:

  • Development of a novel mouse model with an activating PDGFRβ mutation.
  • Induction of atherosclerosis in hypercholesterolemic ApoE(-/-) or Ldlr(-/-) mice.
  • Genetic deletion of STAT1 in VSMCs to assess its role in PDGFRβ-mediated effects.

Main Results:

  • Increased PDGFRβ signaling in VSMCs induced chemokine secretion and leukocyte infiltration in the aorta.
  • The PDGFRβ(D849V) mutation accelerated atherosclerosis progression in hypercholesterolemic mice.
  • Advanced plaques formed in new locations, including the thoracic aorta and coronary arteries.
  • Deletion of STAT1 in VSMCs significantly reduced arterial inflammation and atherosclerotic plaque burden.

Conclusions:

  • PDGFRβ pathway activation profoundly impacts vascular disease development.
  • Inflammation in the outer arterial layers is a critical driver of atherosclerosis.
  • Targeting PDGFRβ-STAT1 signaling in VSMCs represents a potential therapeutic strategy for atherosclerosis.

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