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Matrix Metalloproteinase (MMP)-3 Activates MMP-9 Mediated Vascular Smooth Muscle Cell Migration and Neointima Formation in Mice
Author(s) -
Jason L. Johnson,
Amrita Dwivedi,
Michelle Somerville,
Sarah J. George,
Andrew C. Newby
Publication year - 2011
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.111.225623
Subject(s) - neointima , matrix metalloproteinase , knockout mouse , vascular smooth muscle , cell migration , microbiology and biotechnology , extracellular matrix , gene knockdown , chemistry , cell , biology , medicine , endocrinology , restenosis , receptor , apoptosis , biochemistry , smooth muscle , stent
Several matrix metalloproteinases (MMPs) have been implicated in extracellular matrix destruction and other actions that lead to plaque rupture and myocardial infarction. Conversely, other MMPs have been shown to promote vascular smooth muscle cell (VSMC)-driven neointima formation, which contributes to restenosis, fibrous cap formation, and plaque stability. MMP-3 knockout reduced VSMC accumulation in mouse atherosclerotic plaques, implicating MMP-3 in neointima formation. We therefore investigated the effect of MMP-3 knockout on neointima formation after carotid ligation in vivo and VSMC migration in vitro.

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