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Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

Complement C5a inhibition reduces atherosclerosis in ApoE-/- mice

Helga D Manthey1, Anita C Thomas, Ian A Shiels

  • 1School of Biomedical Sciences, The University of Queensland, Brisbane, Queensland, Australia. helga.manthey@uni-wuerzburg.de

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|April 15, 2011
PubMed

Insights

The complement C5a receptor (CD88) plays a role in atherosclerosis. Blocking CD88 with PMX53 reduced atherosclerotic lesion size and lipid content in mice, suggesting its potential as an antiatherosclerotic drug.

Area of Science:

  • Immunology
  • Cardiovascular Research
  • Pharmacology

Background:

  • The complement C5a receptor, CD88, is found in human atherosclerotic plaques.
  • The specific role of C5a in the development of atherosclerosis (atherogenesis) is not well understood.

Purpose of the Study:

  • To investigate the role of C5a and its receptor CD88 in atherogenesis.
  • To evaluate the therapeutic potential of a CD88 antagonist in a mouse model of atherosclerosis.

Main Methods:

  • Real-time PCR was used to measure aortic CD88 and C5L2 mRNA expression in ApoE(-/-) mice.
  • Immunohistochemistry confirmed CD88 expression on plaque cells.
  • ApoE(-/-) mice were treated with the CD88 antagonist PMX53 to assess its effects on lesion development.

Main Results:

  • Aortic CD88 mRNA expression increased with age in ApoE(-/-) mice, correlating with atherosclerotic lesion development.
  • CD88 was localized to macrophages, smooth muscle cells, and activated endothelial cells within plaques.
  • PMX53 treatment significantly reduced atherosclerotic lesion size and lipid content by approximately 40%.

Conclusions:

  • C5a appears to have a proatherogenic role in the development of atherosclerosis.
  • The CD88 antagonist PMX53 demonstrates potential as an antiatherosclerotic therapeutic agent.

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