Ephrin-Bs drive junctional downregulation and actin stress fiber disassembly to enable wound re-epithelialization

Nunan, Robert, Campbell, Jessica, Mori, Ryoichi, Pitulescu, Mara E., Jiang, Wen Guo ORCID: https://orcid.org/0000-0002-3283-1111, Harding, Keith Gordon, Adams, Ralf H., Nobes, Catherine D. and Martin, Paul ORCID: https://orcid.org/0000-0002-2665-5086 2015. Ephrin-Bs drive junctional downregulation and actin stress fiber disassembly to enable wound re-epithelialization. Cell Reports 13 (7) , pp. 1380-1395. 10.1016/j.celrep.2015.09.085

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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.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Medicine
Subjects:	R Medicine > R Medicine (General)
Publisher:	Cell Press
ISSN:	2211-1247
Date of First Compliant Deposit:	2 October 2017
Date of Acceptance:	30 September 2015
Last Modified:	05 May 2023 01:43
URI:	https://orca.cardiff.ac.uk/id/eprint/81024

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