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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

TRAIL-deficiency accelerates vascular calcification in atherosclerosis via modulation of RANKL

Belinda A Di Bartolo1, Siân P Cartland, Hanis H Harith

  • 1Centre for Vascular Research, University of New South Wales, Sydney, NSW, Australia.

Plos One
|September 17, 2013
PubMed

Insights

TNF-related apoptosis-inducing ligand (TRAIL) deficiency accelerates vascular calcification and cartilaginous metaplasia in atherosclerosis. TRAIL regulates receptor activator of nuclear factor-κB ligand (RANKL) and inflammatory markers involved in vascular bone turnover.

Area of Science:

  • Vascular Biology
  • Bone Homeostasis
  • Atherosclerosis Research

Background:

  • The osteoprotegerin (OPG) and receptor activator of nuclear factor-κB ligand (RANKL) system regulates bone homeostasis and vascular calcification.
  • TNF-related apoptosis-inducing ligand (TRAIL) is a second OPG ligand with an unestablished role in vivo vascular calcification.

Purpose of the Study:

  • To investigate the role of TRAIL in vascular calcification in vitro and in vivo.
  • To examine the involvement of OPG and RANKL in TRAIL-mediated vascular calcification.

Main Methods:

  • In vitro studies used vascular smooth muscle cells (VSMCs) from TRAIL(-/-) and wild-type mice.
  • In vivo studies utilized TRAIL(-/-)ApoE(-/-) mice with advanced atherosclerotic lesions.
  • Analysis included calcium-induced calcification, gene expression (RANKL, OPG, TRAIL, collagen II, BMP-2, IL-1β, PPAR-γ), and histological assessment.

Main Results:

  • TRAIL inhibited calcium-induced calcification in human VSMCs; TRAIL(-/-) VSMCs showed accelerated calcification.
  • TRAIL deficiency in mice led to increased chondrocyte-like cells, collagen II, RANKL, BMP-2, IL-1β, and PPAR-γ expression in atherosclerotic lesions.
  • Significant increases in vascular calcification were observed in TRAIL(-/-)ApoE(-/-) mice.

Conclusions:

  • TRAIL deficiency accelerates cartilaginous metaplasia and vascular calcification in atherosclerosis.
  • TRAIL plays a crucial role in regulating RANKL and inflammatory mediators of vascular bone turnover.

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