Journal
JOURNAL OF CELL BIOLOGY
Volume 203, Issue 2, Pages 327-343Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201305074
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Funding
- National Institute of Dental and Craniofacial Research [DE019108]
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Keratinocyte mobilization is a critical aspect of wound re-epithelialization, but the mechanisms that control its precise regulation remain poorly understood. We set out to test the hypothesis that forkhead box O1 (FOXO1) has a negative effect on healing because of its capacity to inhibit proliferation and promote apoptosis. Contrary to expectations, FOXO1 is required for keratinocyte transition to a wound-healing phenotype that involves increased migration and up-regulation of transforming growth factor beta 1 (TGF-beta 1) and its downstream targets, integrin-alpha 3 and -beta 6 and MMP-3 and -9. Furthermore, we show that FOXO1 functions in keratinocytes to reduce oxidative stress, which is necessary to maintain cell migration and prevent cell death in a TGF-beta 1-independent manner. Thus, our studies identify a novel function for FOXO1 in coordinating the response of keratinocytes to wounding through up-regulation of TGF-beta 1 and other factors needed for keratinocyte migration and protection against oxidative stress, which together promote migration and decrease apoptosis.
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