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  3. Targeted Disruption Of The Scavenger Receptor And Chemokine Cxcl16 Accelerates Atherosclerosis.
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  3. Targeted Disruption Of The Scavenger Receptor And Chemokine Cxcl16 Accelerates Atherosclerosis.

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Targeted disruption of the scavenger receptor and chemokine CXCL16 accelerates atherosclerosis.

Ara M Aslanian1, Israel F Charo

  • 1Gladstone Institute of Cardiovascular Disease, 1650 Owens St, San Francisco, Calif 94158, USA.

Circulation
|August 2, 2006

View abstract on PubMed

Summary
This summary is machine-generated.

CXCL16 acts as a protective scavenger receptor in atherosclerosis, reducing oxidized LDL uptake by macrophages. Its absence accelerates plaque formation and inflammation in mice.

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Area of Science:

  • Immunology
  • Cardiovascular Biology
  • Molecular Medicine

Background:

  • Macrophage scavenger receptors mediate oxidized low-density lipoprotein (OxLDL) uptake, contributing to foam cell formation in atherosclerosis.
  • CXCL16 functions as a scavenger receptor for OxLDL and a chemoattractant for T helper 1 cells, with expression in human and mouse atheroma.
  • These characteristics suggest a role for CXCL16 in the development of atherosclerosis.

Purpose of the Study:

  • To investigate the role of CXCL16 in atherosclerotic plaque formation.
  • To determine the in vivo function of CXCL16 as a scavenger receptor.

Main Methods:

  • Generated CXCL16-deficient (CXCL16-/-) mice and bred them with LDL receptor-deficient (LDLR-/-) mice.
  • Assessed OxLDL binding and internalization by macrophages from CXCL16-/- mice in vitro.
  • Analyzed atherosclerosis progression, macrophage recruitment, and inflammatory gene expression in CXCL16-/-/LDLR-/- mice.

Main Results:

  • Macrophages from CXCL16-/- mice showed significantly reduced capacity to bind and internalize OxLDL.
  • CXCL16-/-/LDLR-/- mice exhibited accelerated atherosclerosis.
  • Increased macrophage recruitment to the aortic arch and elevated mRNA levels for monocyte chemotactic protein-1 and tumor necrosis factor-alpha were observed.

Conclusions:

  • CXCL16 scavenger receptor activity in vivo is atheroprotective.
  • These findings contrast with studies showing protection in scavenger receptor class A- and CD36-deficient mice.
  • CXCL16 plays a significant role in modulating atherosclerosis development through its scavenger receptor function.