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Updated: Jun 17, 2026

A Model of Disturbed Flow-Induced Atherosclerosis in Mouse Carotid Artery by Partial Ligation and a Simple Method of RNA Isolation from Carotid Endothelium
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A Model of Disturbed Flow-Induced Atherosclerosis in Mouse Carotid Artery by Partial Ligation and a Simple Method of RNA Isolation from Carotid Endothelium

Published on: June 22, 2010

An imbalance between CD36 and ABCA1 protein expression favors lipid accumulation in stroke-prone ulcerated carotid

Pia M Isoviita1, Krista Nuotio, Jani Saksi

  • 1Research Program of Molecular Neurology, Biomedicum Helsinki, Helsinki, Finland. pia.isoviita@helsinki.fi

Stroke
|January 9, 2010
PubMed

Insights

An imbalance of CD36 and ABCA1 in carotid plaques (CP) promotes lipid accumulation and instability. CD36

Area of Science:

  • Cardiovascular Biology
  • Atherosclerosis Research
  • Macrophage Biology

Background:

  • CD36 facilitates modified lipoprotein uptake; ABCA1 promotes lipid efflux.
  • Previous microarray data indicated CD36 and ABCA1 gene overexpression in symptomatic carotid plaques (CP).
  • This study investigates the roles of CD36 and ABCA1 in CP destabilization.

Purpose of the Study:

  • To evaluate the role of CD36 and ABCA1 in carotid plaque destabilization.
  • To examine the localization of lipids, CD36, ABCA1, extravasated red blood cells, and necrotic tissue in CP.

Main Methods:

  • Analysis of 92 high-grade stenosing carotid endarterectomy specimens.
  • Oil-red-O staining for neutral lipids.
  • Immunohistochemical analysis of CD36 and ABCA1 in symptomatic and nonsymptomatic CP.

Main Results:

  • Symptomatic CP showed increased extracellular lipid and CD36 expression compared to nonsymptomatic CP.
  • CD36 expression was higher than ABCA1 in ulcerated CP, with the reverse in nonulcerated CP.
  • CD36 colocalized with extravasated red blood cells and necrotic areas, suggesting a role in intraplaque hemorrhage.

Conclusions:

  • An imbalance favoring CD36 (lipid influx) over ABCA1 (lipid efflux) contributes to macrophage lipid accumulation and ulcerated CP destabilization.
  • CD36's colocalization with red blood cells indicates intraplaque hemorrhage may increase lipid load and affect CP stability.
Abstract

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