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|dc.identifier.citation||Experimental Cell Research, 2008; 314(11-12):2165-2175||-|
|dc.description.abstract||Previous studies showed that CD151-null mice have a skin wound healing deficit. To gain an understanding of the role of CD151 in re-epithelialisation and dermal contraction, keratinocyte and fibroblast functions were assayed. Primary CD151-null keratinocytes displayed defective migration on Matrigel (a basement membrane equivalent) and laminin-332, the primary adhesion component of basement membranes, but not on collagen-I. Adhesion, spreading and proliferation were also deficient on laminin-332, but not collagen-I. The data suggest that loss of CD151 impairs the function of its primary interaction partners, integrin alpha3beta1- and/or alpha6beta4 which bind to laminin-332. Skin fibroblasts also produce CD151 mRNA. CD151-null fibroblasts migrated significantly faster on collagen I than wild type fibroblasts, confirming that they possess functional collagen receptors. However, no significant decrease in the ability of CD151-null fibroblasts to cause contraction in floating collagen gel assays in response to transforming growth factor beta-1 (TGF-beta1) or platelet derived growth factor (PDGF-BB) was observed, nor was there an effect on fibroblast adhesion or proliferation on collagen-I. The data implicate CD151 as a facilitator of laminin-332-mediated keratinocyte functions that impact on the re-epithelialisation process intrinsic to wound healing and further suggest a potential novel role for CD151 in fibroblast migration.||-|
|dc.description.statementofresponsibility||Sean M. Geary, Allison J. Cowin, Ben Copeland, Rosa M. Baleato, Kaoru Miyazaki, Leonie K. Ashman||-|
|dc.publisher||Academic Press Inc Elsevier Science||-|
|dc.subject||Skin wound healing||-|
|dc.title||The role of the tetraspanin CD151 in primary keratinocyte and fibroblast functions: Implications for wound healing||-|
|dc.identifier.orcid||Cowin, A. [0000-0003-2885-2080]||-|
|Appears in Collections:||Aurora harvest|
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