Circulation Research. 2002;91:852-859
Published online before print October 10, 2002, doi: 10.1161/01.RES.0000041036.86977.14
Published online before print October 10, 2002, doi: 10.1161/01.RES.0000041036.86977.14
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© 2002 American Heart Association, Inc.
Integrative Physiology |
Targeted Disruption of the Matrix Metalloproteinase-9 Gene Impairs Smooth Muscle Cell Migration and Geometrical Arterial Remodeling
From the Division of Cardiology (Z.S.G., C.J., D.G., R.M., E.I.), Emory University School of Medicine, Atlanta, Ga; the Department of Biomedical Engineering (Z.S.G., C.J., R.M.), Emory University/Georgia Institute of Technology, Atlanta, Ga; and the Pulmonary and Critical Care Division, Department of Medicine and Department of Cell Biology and Physiology (J.M.S., R.M.S.), Washington University School of Medicine, St Louis, Mo.
Correspondence to Zorina S. Galis, PhD, Depts of Medicine and Biomedical Engineering, Emory University School of Medicine, 1639 Pierce Dr, WMB 319, Atlanta GA 30322. E-mail zgalis{at}emory.edu
Matrix remodeling plays an important role in the physiological and pathological remodeling of blood vessels. We specifically investigated the role of matrix metalloproteinase (MMP)-9, an MMP induced during arterial remodeling, by assessing the effects of genetic MMP-9 deficiency on major parameters of arterial remodeling using the mouse carotid artery flow cessation model. Compared with remodeling of matched wild-type (WT) arteries, MMP-9 deficiency decreased intimal hyperplasia, reduced the late lumen loss, eliminated the correlation between intimal hyperplasia and geometric remodeling, and led to significant accumulation of interstitial collagen. Biochemical analysis of MMP-9 knockout (KO) arterial tissue and isolated smooth muscle cells (SMCs) confirmed the lack of MMP-9 expression or compensation by other gelatinases. To investigate potential mechanisms for the in vivo observations, we analyzed in vitro effects of MMP-9 deficiency on the migration, proliferation, and collagen gel contracting capacity of aortic SMCs isolated from MMP-9 KO and WT mice. Although proliferation was comparable, we found that MMP-9-deficient cells had not only decreased migratory activity, but they also had decreased capacity to contract collagen compared with WT cells. Thus, MMP-9 appears to be involved not only in degradation, but also in reorganization of a collagenous matrix, both facets being essential for the outcome of arterial remodeling. Our results also establish MMP-9 as an attractive therapeutic target for limiting the effects of pathological arterial remodeling in restenosis and atherosclerosis.
Key Words: matrix degradation • cell migration • restenosis • atherosclerosis
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M. Kuzuya, S. Kanda, T. Sasaki, N. Tamaya-Mori, X. W. Cheng, T. Itoh, S. Itohara, and A. Iguchi Deficiency of Gelatinase A Suppresses Smooth Muscle Cell Invasion and Development of Experimental Intimal Hyperplasia Circulation, September 16, 2003; 108(11): 1375 - 1381. [Abstract] [Full Text] [PDF]
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A. Castrillo, S. B. Joseph, C. Marathe, D. J. Mangelsdorf, and P. Tontonoz Liver X Receptor-dependent Repression of Matrix Metalloproteinase-9 Expression in Macrophages J. Biol. Chem., March 14, 2003; 278(12): 10443 - 10449. [Abstract] [Full Text] [PDF]
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