| First Author | Ponugoti B | Year | 2013 |
| Journal | J Cell Biol | Volume | 203 |
| Issue | 2 | Pages | 327-43 |
| PubMed ID | 24145170 | Mgi Jnum | J:208099 |
| Mgi Id | MGI:5560888 | Doi | 10.1083/jcb.201305074 |
| Citation | Ponugoti B, et al. (2013) FOXO1 promotes wound healing through the up-regulation of TGF-beta1 and prevention of oxidative stress. J Cell Biol 203(2):327-43 |
| abstractText | 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 beta1 (TGF-beta1) and its downstream targets, integrin-alpha3 and -beta6 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-beta1-independent manner. Thus, our studies identify a novel function for FOXO1 in coordinating the response of keratinocytes to wounding through up-regulation of TGF-beta1 and other factors needed for keratinocyte migration and protection against oxidative stress, which together promote migration and decrease apoptosis. |
