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Updated: Jun 2, 2026
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
Summary
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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