© 1997 American Heart Association, Inc.
Articles |
Immunohistochemical Colocalization of the Terminal Complex of Human Complement and Smooth Muscle Cell 
-Actin in Early Atherosclerotic Lesions
From the Institute of Pathology, Heinrich-Heine-University Düsseldorf, Germany, and the Department of Cardiology, University of Ulm, Germany (J.T., J.W., V.H.), and the Department of Pathology, University of Cambridge, Cambridge, UK (D.E.B., C.F.)
Correspondence to Dr David Bowyer, University of Cambridge, Department of Pathology, Division of Cellular Pathology, Tennis Court Road, Cambridge CB2 1QP, England. E-mail david.bowyer{at}mole.bio.cam.ac.uk.
Abstract There is substantial evidence that activated
components of the complement cascade are present in atherosclerotic
lesions, and it was suggested some years ago that smooth muscle cells
may be an important target of complement attack by the terminal
components of the cascade, C5b-9, also called the membrane attack
complex. Recent in vitro studies have shown that assembly of membrane
attack complex on smooth muscle cells leads to the release of monocyte
chemotactic protein-1, and, if this were to occur in vivo, then it
could be responsible for the recruitment of monocytes into the lesion.
In this study we have investigated the localization of C5b-9 in early
atherosclerotic lesions of human coronary arteries, collected
from autopsies, by immunohistochemical staining. C5b-9 was found to
colocalize widely with smooth muscle cell -actin, but not with
intact macrophages, thus supporting the hypothesis that
interaction of complement with smooth muscle cells may indeed be
important in atherogenesis.
Key Words: atherogenesis • C5b-9 • early lesions • complement
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