© 1997 American Heart Association, Inc.
Articles |
Collagen VIII Is Expressed by Vascular Smooth Muscle Cells in Response to Vascular Injury
From the Cardiovascular Biology Laboratory, Harvard School of Public Health (N.E.S.S., L.C.F., C.-M.H., M.A.P., W.-S.L., W.O.E., M.-E.L., E.H.), the Department of Medicine, Harvard Medical School (N.E.S.S., M.A.P., M.-E.L., E.H.), and the Cardiovascular (N.E.S.S., M.-E.L.) and Pulmonary (M.A.P.) Divisions, Brigham and Women's Hospital, Boston, Mass, and the Department of Biological Structure, University of Washington School of Medicine (E.H.S.), Seattle, Wash.
Correspondence to Edgar Haber, MD, Cardiovascular Biology Laboratory, Harvard School of Public Health, 677 Huntington Ave, Boston, MA 02115. E-mail haber{at}cvlab.harvard.edu
Abstract To identify genes involved in vascular remodeling,
we applied differential mRNA display analysis to the rat carotid artery
balloon injury model. One polymerase chain reaction product showing
increased expression at days 2 to 14 after vascular injury was nearly
identical to the mouse 
1 chain of type VIII collagen, a
heterotrimeric short-chain collagen of uncertain function expressed by
a limited number of cell types. By Northern analysis, expression of
both chains of the type VIII collagen heterotrimer increased: collagen
1 (VIII) mRNA expression was almost 4-fold higher than
control by 7 days after vascular injury, and collagen 2
(VIII) mRNA expression reached a maximum of almost 6-fold above
baseline by 3 days after injury. By immunohistochemical analysis, type
VIII collagen expression increased in the media and neointima in a
localized pattern consistent with the distribution of activated
dedifferentiated vascular smooth muscle cells (VSMCs). Cultured VSMCs
expressed higher levels of type VIII collagen in response to serum and
growth factors, notably platelet-derived growth factor (PDGF)-BB. VSMCs
adhered significantly less to type VIII collagen than to type I
collagen substrata and showed greater PDGF-BB–stimulated migration (by
2.2-fold) on type VIII collagen than on type I collagen. We hypothesize
that increased expression of type VIII collagen by VSMCs after
arterial injury may contribute to vascular remodeling through the
promotion of VSMC migration.
Key Words: cardiovascular disease • artery • gene expression • extracellular matrix • cell movement
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