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Published on: May 6, 2014

The involvement of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in atherosclerosis

Yoav Michowitz1, Emil Goldstein, Arie Roth

  • 1Department of Cardiology, Tel Aviv Sourasky Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.

Journal of the American College of Cardiology
|April 6, 2005
PubMed

Insights

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is found in atherosclerotic plaques and induced by oxidized LDL. Soluble TRAIL levels are lower in patients with acute coronary syndromes, suggesting a role in atherosclerosis.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Inflammation is a key factor in atherosclerosis development.
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a TNF superfamily member involved in apoptosis and immune modulation.

Purpose of the Study:

  • To investigate the role and significance of TRAIL in atherosclerotic vascular disease.
  • To determine TRAIL expression and its regulation in atherosclerotic plaques and relevant cells.

Main Methods:

  • Assayed TRAIL presence in human atherosclerotic plaques and mouse aortas.
  • Examined TRAIL inducibility in peripheral mononuclear cells exposed to oxidized LDL (oxLDL) via immunoblot and RT-PCR.
  • Measured soluble TRAIL levels in patients using ELISA.

Main Results:

  • TRAIL was present in stable lesions and elevated in vulnerable plaques, co-localizing with CD3 cells and oxLDL.
  • TRAIL mRNA and protein expression increased in PBMCs after oxLDL incubation.
  • Soluble TRAIL levels were significantly reduced in unstable angina patients compared to stable patients and healthy controls.

Conclusions:

  • TRAIL is expressed in plaque-infiltrating CD3 cells and induced by oxLDL.
  • Reduced soluble TRAIL levels in acute coronary syndromes correlate negatively with C-reactive protein.
  • These findings suggest a potential role for TRAIL in the pathogenesis of atherosclerosis.
Abstract

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