© 2000 American Heart Association, Inc.
Vascular Biology |
Mitogen-Activated Protein Kinases Mediate Matrix Metalloproteinase-9 Expression in Vascular Smooth Muscle Cells
From the Department of Pathology (A.C., M.A.R.) and the Department of Immunology (J.G.), University of Washington, Seattle.
Correspondence to Aesim Cho, PhD, Department of Pathology, Box 357335, University of Washington, Seattle, WA 98195. E-mail ascho{at}u.washington.edu
Abstract—Expression
of matrix metalloproteinase (MMP)-9 has been linked to the progression
of plaque rupture and intimal formation in arterial
lesions. In this study, we determined which factors and signaling
pathways are involved in regulating the MMP-9 gene. Rat carotid
arterial smooth muscle cells treated with tumor necrosis
factor (TNF)-
showed a marked increase in MMP-9 activity and mRNA
level, whereas platelet-derived growth factor (PDGF) showed a
slight induction of the MMP-9 mRNA level. TNF- treatment caused an
increase in c-Jun N-terminal kinase (JNK), p38
mitogen-activated protein kinase (p38 MAPK), and extracellular
signal–regulated kinase (ERK) activities, whereas PDGF treatment
caused an increase in ERKs and p38 MAPK activities without any effect
on JNK activity. Treatment with either SB203580 (inhibitor
of p38 MAPK) or U0126 (inhibitor of the ERK pathway)
downregulated the TNF-–induced MMP-9 expression in a dose-dependent
manner. Treatment of cells with TNF- and PDGF together stimulated
the MMP-9 expression at a level higher than that observed with either
factor alone, suggesting that TNF- and PDGF have a synergistic
effect on MMP-9 expression in arterial smooth muscle cells.
Furthermore, suboptimal inhibitory concentrations of
SB203580 and U0126 together almost completely inhibited the MMP-9
expression. These results suggest that p38 MAPK and ERK pathways
contribute to the transcriptional regulation of MMP-9 in
arterial smooth muscle cells.
Key Words: mitogen-activated protein kinases • p38 mitogen-activated protein kinase • extracellular signal–regulated kinase • matrix metalloproteinase-9 • tumor necrosis factor
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