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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

Calcification is associated with loss of functional calcium-sensing receptor in vascular smooth muscle cells

Masih-ul Alam1, John Paul Kirton, Fiona L Wilkinson

  • 1Wellcome Trust Centre for Cell-Matrix Research, University of Manchester, Michael Smith Building, Oxford Road, Manchester M139PT, UK.

Cardiovascular Research
|October 15, 2008
PubMed
Abstract

Insights

Calcimimetics reduce vascular calcification by targeting the calcium-sensing receptor (CaR) in vascular smooth muscle cells (VSMCs). This suggests a potential therapeutic strategy for chronic kidney disease patients at risk of vascular complications.

Area of Science:

  • Vascular Biology
  • Nephrology
  • Pharmacology

Background:

  • Vascular calcification (VC) is a significant risk factor for morbidity and mortality in advanced chronic kidney disease (CKD).
  • Calcimimetics, which modulate the calcium-sensing receptor (CaR), have shown promise in inhibiting VC in animal models.
  • The role of CaR in vascular smooth muscle cells (VSMCs) and its potential as a therapeutic target for VC require further investigation.

Purpose of the Study:

  • To investigate the expression of CaR in the vasculature.
  • To determine the functional role of CaR in VSMCs.
  • To evaluate the efficacy of calcimimetics in preventing VSMC calcification in vitro.

Main Methods:

  • Immunohistochemistry, immunofluorescence, and immunoblotting were used to detect CaR expression in human arteries and VSMCs.
  • VSMCs were stimulated with varying calcium concentrations and CaR agonists/antagonists.
  • Mineral deposition and extracellular signal-regulated kinase (ERK1/2) phosphorylation were assessed to evaluate CaR function and calcification.

Main Results:

  • CaR protein is expressed in VSMCs of normal arteries but reduced in calcified arteries.
  • VSMC CaR expression decreases with matrix deposition and increased calcium levels.
  • Calcimimetics, such as R-568, attenuated VSMC mineral deposition, while CaR over-expression enhanced it.

Conclusions:

  • VSMCs express a functional CaR, and its reduced expression is linked to increased mineralization.
  • Calcimimetics effectively decrease mineral deposition in VSMCs.
  • These findings suggest that calcimimetics hold potential for inhibiting VC in CKD patients.

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