α3β1 integrin–controlled Smad7 regulates reepithelialization during wound healing in mice

Reynolds, Louise E., Conti, Francesco J., Silva, Rita, Robinson, Stephen D. ORCID: https://orcid.org/0000-0002-6606-7588, Iyer, Vandana, Rudling, Rob, Cross, Barbara, Nye, Emma, Hart, Ian R., DiPersio, C. Michael and Hodivala-Dilke, Kairbaan M. (2008) α3β1 integrin–controlled Smad7 regulates reepithelialization during wound healing in mice. Journal of Clinical Investigation, 118 (3). pp. 965-974. ISSN 0021-9738

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Abstract

Effective reepithelialization after injury is essential for correct wound healing. The upregulation of keratinocyte a3ß1 integrin during reepithelialization suggests that this adhesion molecule is involved in wound healing; however, its precise role in this process is unknown. We have shown here that retarded reepithelialization in Itga3–/– mouse skin wounds is due predominantly to repressed TGF-ß1–mediated responses. Specifically, expression of the inhibitor of TGF-ß1–signaling Smad7 was elevated in Itga3–/– keratinocytes. Indeed, in vivo blockade of Smad7 increased the rate of reepithelialization in Itga3–/– and WT wounds to similar levels. Our data therefore indicate that the function of a3ß1 integrin as a mediator of keratinocyte migration is not essential for reepithelialization but suggest instead that a3ß1 integrin has a major new in vivo role as an inhibitor of Smad7 during wound healing. Moreover, our study may identify a previously undocumented function for Smad7 as a regulator of reepithelialization in vivo and implicates Smad7 as a potential novel target for the treatment of cutaneous wounds.

Item Type:	Article
Faculty \ School:	Faculty of Science > School of Biological Sciences
Depositing User:	Users 2731 not found.
Date Deposited:	22 Nov 2011 14:10
Last Modified:	23 Oct 2022 05:40
URI:	https://ueaeprints.uea.ac.uk/id/eprint/35537
DOI:	10.1172/JCI33538

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