Does C5a have a role in the pathophysiology of atherosclerosis?

Manthey, H., Taylor, S., Shiels, I. and Rolfe, B. (2007). Does C5a have a role in the pathophysiology of atherosclerosis?. In: W.-C. Song and X.-M. Gao, Molecular Immunology: Proceedings XXI International Complement Workshop. XXI International Complement Workshop, Beijing, China, (213-213). 22-26 October 2006. doi:10.1016/j.molimm.2006.07.154

Author Manthey, H.
Taylor, S.
Shiels, I.
Rolfe, B.
Title of paper Does C5a have a role in the pathophysiology of atherosclerosis?
Conference name XXI International Complement Workshop
Conference location Beijing, China
Conference dates 22-26 October 2006
Proceedings title Molecular Immunology: Proceedings XXI International Complement Workshop   Check publisher's open access policy
Journal name Molecular Immunology   Check publisher's open access policy
Place of Publication Oxford, United Kingdom
Publisher Pergamon
Publication Year 2007
Year available 2006
Sub-type Published abstract
DOI 10.1016/j.molimm.2006.07.154
ISSN 0161-5890
Editor W.-C. Song
X.-M. Gao
Volume 44
Issue 1-3
Start page 213
End page 213
Total pages 1
Collection year 2007
Language eng
Formatted Abstract/Summary
Activation of the complement system contributes to the pathogenesis and progression of most cardiovascular diseases, including atherosclerosis. There is mounting evidence supporting a role for the complement activation product 5a (C5a) and its receptor (C5aR) in the pathogenesis of atherosclerosis. To determine whether C5a may play a role in atherosclerosis, in vivo and in vitro models of atherosclerosis pathology were utilized.
     An ApoE knockout (ApoE KO) mouse model of atherosclerosis was used to examine C5aR mRNA expression in the heart, aorta, kidney and liver from 25-week-old ApoE KO mice and the wild-type, C57BL/6. C5aR mRNA expression was detected in all tissues using RT-PCR, however there was no difference in expression between ApoE KO mice and the wild-type. Current studies are examining changes in C5aR mRNA expression with lesion progression from ApoE KO and wild-type mice at 3, 5, 9, 12 and 17 weeks of age.
     Vascular smooth muscle cells (VSMC), harvested and seeded into primary culture, undergo a spontaneous change from a contractile to a synthetic phenotype after 6–8 days. Similarly, this occurs in VSMC in atherosclerotic lesions, where cells in the synthetic phenotype are capable of proliferating, migrating and secreting extracellular matrix. We have found that VSMC harvested from female Wistar rats and in the synthetic phenotype, express C5aR mRNA. Functional cell surface C5aRs are being determined by protein expression in rat VSMC using Western blot. To determine any direct effect of C5a, we have stimulated rat VSMC with C5a or a peptide C5a agonist and shown that C5a agonists do not affect VSMC proliferation in the presence of serum mitogens.
     These findings suggest that C5a has the potential to play a role in atherosclerosis, however further studies are required to clarify the precise role that it may play.
Subjects 1102 Cardiovascular Medicine and Haematology
Keyword Biochemistry & molecular biology
Q-Index Code CX
Q-Index Status Provisional Code
Institutional Status UQ
Additional Notes Abstract no. 149

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Created: Mon, 18 Feb 2008, 15:54:26 EST