| First Author | Sano Y | Year | 2014 |
| Journal | J Invest Dermatol | Volume | 134 |
| Issue | 8 | Pages | 2231-2240 |
| PubMed ID | 24662766 | Mgi Jnum | J:212839 |
| Mgi Id | MGI:5582340 | Doi | 10.1038/jid.2014.153 |
| Citation | Sano Y, et al. (2014) Loss of epidermal p38alpha signaling prevents UVR-induced inflammation via acute and chronic mechanisms. J Invest Dermatol 134(8):2231-40 |
| abstractText | UVB is a component of solar radiation primarily responsible for causing damage and cancer in irradiated skin, and disrupting immune homeostasis. The immediate harm and long-term health risks of excessive sunlight exposure are affecting the lives of nearly all people worldwide. Inflammation is a key mechanism underlying UVB's various detrimental effects. Here we show that activation of the protein kinase p38alpha is restricted to the epidermis in UVB-exposed skin, and that p38alpha ablation targeted to the epithelial compartment is sufficient to suppress UVB-induced inflammation. Mechanistically, loss of epithelial p38alpha signaling attenuates the expression of genes required to induce vascular leakage and edema, and also increases the steady-state abundance of epidermal gammadelta T cells, which are known to promote the repair of damaged epidermis. These effects of p38alpha deficiency delineate a molecular network operating at the organism-environment interface, and reveal conditions crucial to preventing the pathology resulting from sun-damaged skin. |
