© 2001 American Heart Association, Inc.
Molecular Medicine |
Fibrillar Collagen Specifically Regulates Human Vascular Smooth Muscle Cell Genes Involved in Cellular Responses and the Pericellular Matrix Environment
From the Departments of Biochemistry (T.I., S.O.), Internal Medicine (H.K., S.T., Y.N.), Pharmacology (S.K., H.I.), and Cardiovascular Medicine (A.S., Y.O.), Osaka City University Medical School, Osaka, Japan, and Department of Pathology (E.W.R.), University of Washington, Seattle, Wash.
Correspondence to Hidenori Koyama, MD, PhD, Second Department of Internal Medicine, Osaka City University Medical School, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan. E-mail hidekoyama{at}med.osaka-cu.ac.jp
Abstract—Proliferation
and 
vß3
integrin–dependent migration of vascular smooth muscle cells are
suppressed on polymerized type I collagen. To identify genes
specifically regulated in human smooth muscle cells by polymerized
collagen, we used the suppressive subtraction hybridization technique.
Compared with smooth muscle cells cultured on monomer collagen,
polymerized collagen suppresses the following: (1) a number of other
extracellular matrix proteins, including fibronectin, thrombospondin-1,
tenascin-C, and cysteine-rich protein 61; (2) actin binding proteins
including -actinin; (3) signaling molecules; (4) protein
synthesis–associated proteins; and (5) genes with unknown functions.
Some of the identified genes, including cysteine-rich protein 61, show
unique kinetics of mRNA regulation by monomer or polymerized collagen
distinct from growth factors, suggesting extracellular matrix–specific
gene modulation. Moreover, in vivo balloon catheter–mediated injury to
the rat carotid artery induces many of the genes that are suppressed by
polymerized collagen. Protein levels of thrombospondin-1 and
fibronectin are also suppressed by polymerized collagen.
Thrombospondin-1–mediated smooth muscle cell migration on vitronectin
is significantly inhibited after culture on polymerized collagen for 24
hours, which is associated with decreased -actinin accumulation at
focal adhesions. Thus, polymerized type I collagen dynamically
regulates gene expression, pericellular accumulation of extracellular
matrix molecules, and the response to a given matrix
molecule.
Key Words: thrombospondin-1 • platelet-derived growth factor • -actinin • filamin • balloon injury
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