Source:http://linkedlifedata.com/resource/pubmed/id/20940256
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
Pt 21
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pubmed:dateCreated |
2010-10-25
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pubmed:abstractText |
In tissue repair, fibroblasts migrate into the wound to produce and remodel extracellular matrix (ECM). Integrins are believed to be crucial for tissue repair, but their tissue-specific role in this process is poorly understood. Here, we show that mice containing a fibroblast-specific deletion of integrin ?1 exhibit delayed cutaneous wound closure and less granulation tissue formation, including reduced production of new ECM and reduced expression of ?-smooth muscle actin (?-SMA). Integrin-?1-deficient fibroblasts showed reduced expression of type I collagen and connective tissue growth factor, and failed to differentiate into myofibroblasts as a result of reduced ?-SMA stress fiber formation. Loss of integrin ?1 in adult fibroblasts reduced their ability to adhere to, to spread on and to contract ECM. Within stressed collagen matrices, integrin-?1-deficient fibroblasts showed reduced activation of latent TGF?. Addition of active TGF? alleviated the phenotype of integrin-?1-deficient mice. Thus integrin ?1 is essential for normal wound healing, where it acts, at least in part, through a TGF?-dependent mechanism in vivo.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Acta2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Actins,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD29,
http://linkedlifedata.com/resource/pubmed/chemical/Collagen Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Connective Tissue Growth Factor
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1477-9137
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
123
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3674-82
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pubmed:dateRevised |
2011-7-15
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pubmed:meshHeading |
pubmed-meshheading:20940256-Actins,
pubmed-meshheading:20940256-Animals,
pubmed-meshheading:20940256-Antigens, CD29,
pubmed-meshheading:20940256-Cell Differentiation,
pubmed-meshheading:20940256-Cells, Cultured,
pubmed-meshheading:20940256-Collagen Type I,
pubmed-meshheading:20940256-Connective Tissue Growth Factor,
pubmed-meshheading:20940256-Fibroblasts,
pubmed-meshheading:20940256-Focal Adhesions,
pubmed-meshheading:20940256-Gene Expression Regulation,
pubmed-meshheading:20940256-Humans,
pubmed-meshheading:20940256-Mice,
pubmed-meshheading:20940256-Mice, Knockout,
pubmed-meshheading:20940256-Myofibroblasts,
pubmed-meshheading:20940256-Sequence Deletion,
pubmed-meshheading:20940256-Skin,
pubmed-meshheading:20940256-Stress Fibers,
pubmed-meshheading:20940256-Wound Healing
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pubmed:year |
2010
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pubmed:articleTitle |
Expression of integrin beta1 by fibroblasts is required for tissue repair in vivo.
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pubmed:affiliation |
The Canadian Institute of Health Research Group in Skeletal Development and Remodeling, Division of Oral Biology and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, University of Western Ontario, Dental Sciences Building, London, ON N6A 5C1, Canada.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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