期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 118, 期 3, 页码 965-974出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI33538
关键词
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Effective reepithelialization after injury is essential for correct wound healing. The upregulation of keratinocyte alpha 3 beta 1 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-beta 1-mediated responses. Specifically, expression of the inhibitor of TGF-beta 1-signaling Smad7 was elevated in Itga3(-/-) keratinocytes. Indeed, in vivo blockade of SmaA7 increased the rate of reepithelialization in Itga3(-/-) and WT wounds to similar levels. Our data therefore indicate that the function of alpha 3 beta 1 integrin as a mediator of keratinocyte migration is not essential for reepithelialization but suggest instead that alpha 3 beta 1 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.
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