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Quantification of Atherosclerosis in Mice
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Quantification of Atherosclerosis in Mice

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Loss of SR-A and CD36 activity reduces atherosclerotic lesion complexity without abrogating foam cell formation in

Jennifer J Manning-Tobin1, Kathryn J Moore, Tracie A Seimon

  • 1Lipid Metabolism Unit, Harvard Medical School, Massachusetts General Hospital, Boston, MA 02114, USA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|October 25, 2008
PubMed

Insights

Deleting scavenger receptors SR-A and CD36 in Apoe(-/-) mice did not reduce lesion size but decreased inflammation, macrophage apoptosis, and plaque necrosis, suggesting potential for plaque stabilization.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Atherosclerosis Research

Background:

  • Scavenger receptors SR-A and CD36 are linked to macrophage foam cell formation in atherosclerosis.
  • These receptors also regulate inflammatory pathways involved in plaque necrosis and apoptosis.

Purpose of the Study:

  • To investigate the impact of deleting SR-A and CD36 on atherogenesis.
  • To assess effects on lesion development, inflammation, and plaque stability.

Main Methods:

  • Generated Apoe(-/-) mice lacking both SR-A and CD36 (Apoe(-/-)Cd36(-/-)Msr1(-/-)).
  • Fed mice a Western diet for 12 weeks.
  • Analyzed aortic root atherosclerosis using morphometry, electron microscopy, and immunohistochemistry.

Main Results:

  • No significant reduction in lesion area or foam cell formation was observed compared to Apoe(-/-) mice.
  • Apoe(-/-)Cd36(-/-)Msr1(-/-) lesions showed reduced inflammatory gene expression.
  • Macrophage apoptosis decreased by ~30% and plaque necrosis by ~50%.

Conclusions:

  • Deletion of SR-A and CD36 does not prevent foam cell formation or reduce lesion size in this model.
  • Loss of these receptors significantly reduces macrophage apoptosis and plaque necrosis.
  • Targeting SR-A and CD36 may offer a strategy to promote plaque stability by reducing inflammation and necrosis.
Abstract

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