Ephrin-Bs Drive Junctional Downregulation and Actin Stress Fiber Disassembly to Enable Wound Re-epithelialization

Robert Nunan, Jessica Campbell, Ryoichi Mori, Mara E Pitulescu, Wen G. Jiang, Keith G Harding, Ralf H Adams, Catherine D Nobes, Paul B Martin

Research output: Contribution to journalArticle (Academic Journal)peer-review

31 Citations (Scopus)
363 Downloads (Pure)

Abstract

For a skin wound to successfully heal, the cut epidermal-edge cells have to migrate forward at the interface between scab and healthy granulation tissue. Much is known about how lead-edge cells migrate, but very little is known about the mechanisms that enable active participation by cells further back. Here we show that ephrin-B1 and its receptor EphB2 are both upregulated in vivo, just for the duration of repair, in the first 70 or so rows of epidermal cells, and this signal leads to downregulation of the molecular components of adherens and tight (but not desmosomal) junctions, leading to loosening between neighbors and enabling shuffle room among epidermal cells. Additionally, this signaling leads to the shutdown of actomyosin stress fibers in these same epidermal cells, which may act to release tension within the wound monolayer. If this signaling axis is perturbed, then disrupted healing is a consequence in mouse and man.

Original languageEnglish
Pages (from-to)1380–1395
Number of pages16
JournalCell Reports
Volume13
Issue number7
Early online date5 Nov 2015
DOIs
Publication statusPublished - 17 Nov 2015

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