© 1996 American Heart Association, Inc.
Articles |
Regulation of Matrix Metalloproteinases and Plasminogen Activator Inhibitor-1 Synthesis by Plasminogen in Cultured Human Vascular Smooth Muscle Cells
From the Harvard-MIT Division of Health Sciences and Technology (E.L., A.J.G., R.T.L.), Cambridge, Mass; the Cardiology Division (D.E.V.), Vanderbilt University Medical Center and Veterans Affairs Medical Center, Nashville, Tenn; the Cardiovascular Division (S.H.P., P.L., R.T.L.), Brigham and Women's Hospital, Harvard Medical School, Boston, Mass; and Merck Research Laboratories (M.W.L.), Rahway, NJ.
Correspondence to Richard T. Lee, MD, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115. E-mail rtlee@bics.bwh.harvard.edu.
Abstract Plasmin and matrix metalloproteinases (MMPs) both
participate in extracellular matrix remodeling. This study examined the
effects of tumor necrosis factor-
(TNF-) and
plasminogen on collagenase, stromelysin, and
plasminogen activator inhibitor-1
(PAI-1) synthesis by cultured human vascular smooth muscle cells
(SMCs). TNF- induced the concentration-dependent synthesis of
collagenase and stromelysin, which remained predominantly
in proenzyme forms, as determined by Western analysis of
culture media. In contrast, plasminogen and plasmin not
only increased secretion of MMPs but also induced cleavage to their
active forms. The serine protease inhibitor aprotinin
inhibited this activation of MMPs by plasminogen and
plasmin. TNF- reduced plasminogen-induced activation
of MMPs, suggesting induction of an inhibitor of plasmin
generation, such as PAI-1. Enzyme-linked immunosorbent assay of
culture media showed that TNF- (10 ng/mL) increased PAI-1 secretion
by 4.2-fold compared with control (105.5±9.6 versus 24.9±1.7
ng/mL,
n=3). Surprisingly, plasminogen also increased PAI-1
secretion by vascular SMCs (3.6-fold over control). These results
demonstrate coordination of cytokines and serine proteases in
regulating MMP secretion and activation. In addition, the induction of
PAI-1 by TNF- and plasminogen suggests a
negative-feedback mechanism to limit both plasmin-mediated and
MMP-mediated matrix degradation.
Key Words: collagenase • stromelysin • vascular smooth muscle • plasmin • plasminogen
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