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Title: The role of the tetraspanin CD151 in primary keratinocyte and fibroblast functions: Implications for wound healing

Journal Article · · Experimental Cell Research
 [1];  [2]; ;  [1];  [3];  [1]
  1. School of Biomedical Sciences, University of Newcastle, New South Wales (Australia)
  2. Child Health Research Institute, North Adelaide, South Australia (Australia)
  3. Division of Cell Biology, Kihara Institute for Biological Research, Yokohama City University, Yokohama (Japan)

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 {alpha}3{beta}1- and/or {alpha}6{beta}4 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-{beta}1) 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.

OSTI ID:
21128139
Journal Information:
Experimental Cell Research, Vol. 314, Issue 11-12; Other Information: DOI: 10.1016/j.yexcr.2008.04.011; PII: S0014-4827(08)00172-9; Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0014-4827
Country of Publication:
United States
Language:
English

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