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Dev Cell. 2011 Oct 18;21(4):681-93. doi: 10.1016/j.devcel.2011.08.007. Epub 2011 Oct 6.

A syndecan-4 hair trigger initiates wound healing through caveolin- and RhoG-regulated integrin endocytosis.

Author information

1
School of Biochemistry, University of Bristol, University Walk, Bristol BS8 1TD, UK. mark.bass@bristol.ac.uk

Erratum in

  • Dev Cell. 2012 Nov 13;23(5):1081-2.

Abstract

Cell migration during wound healing requires adhesion receptor turnover to enable the formation and disassembly of cell-extracellular matrix contacts. Although recent advances have improved our understanding of integrin trafficking pathways, it is not known how extracellular ligand engagement controls receptor dynamics. Using atomic force microscopy, we have measured cell avidity for fibronectin and defined a mechanism for the outside-in regulation of α(5)β(1)-integrin. Surprisingly, adhesive strength was attenuated by the syndecan-4-binding domain of fibronectin due to a rapid triggering of α(5)β(1)-integrin endocytosis. Association of syndecan-4 with PKCα was found to trigger RhoG activation and subsequent dynamin- and caveolin-dependent integrin uptake. Like disruption of syndecan-4 or caveolin, gene disruption of RhoG in mice was found to retard closure of dermal wounds due to a migration defect of the fibroblasts and keratinocytes of RhoG null mice. Thus, this syndecan-4-regulated integrin endocytic pathway appears to play a key role in tissue repair.

PMID:
21982645
PMCID:
PMC3202633
DOI:
10.1016/j.devcel.2011.08.007
[Indexed for MEDLINE]
Free PMC Article

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