Source:http://linkedlifedata.com/resource/pubmed/id/12411401
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
9
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| pubmed:dateCreated |
2002-11-4
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| pubmed:abstractText |
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.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Nov
|
| pubmed:issn |
1524-4571
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:day |
1
|
| pubmed:volume |
91
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
852-9
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:12411401-Animals,
pubmed-meshheading:12411401-Carotid Arteries,
pubmed-meshheading:12411401-Carotid Stenosis,
pubmed-meshheading:12411401-Cell Movement,
pubmed-meshheading:12411401-Collagen,
pubmed-meshheading:12411401-Disease Models, Animal,
pubmed-meshheading:12411401-Disease Progression,
pubmed-meshheading:12411401-Electrophoresis, Polyacrylamide Gel,
pubmed-meshheading:12411401-Enzyme Induction,
pubmed-meshheading:12411401-Gelatin,
pubmed-meshheading:12411401-Gene Targeting,
pubmed-meshheading:12411401-Immunohistochemistry,
pubmed-meshheading:12411401-Male,
pubmed-meshheading:12411401-Matrix Metalloproteinase 2,
pubmed-meshheading:12411401-Matrix Metalloproteinase 9,
pubmed-meshheading:12411401-Mice,
pubmed-meshheading:12411401-Mice, Inbred Strains,
pubmed-meshheading:12411401-Mice, Knockout,
pubmed-meshheading:12411401-Muscle, Smooth, Vascular,
pubmed-meshheading:12411401-Vascular Patency
|
| pubmed:year |
2002
|
| pubmed:articleTitle |
Targeted disruption of the matrix metalloproteinase-9 gene impairs smooth muscle cell migration and geometrical arterial remodeling.
|
| pubmed:affiliation |
Division of Cardiology, Dept of Medicine, Emory University School of Medicine, Atlanta, Ga 30322, USA. zgalis@emory.edu
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
|