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• W2088631936 abstract "Background Raf is one of the downstream effectors of Ras GTPases, and plays a key role in regulating cell proliferation and differentiation through the activation of MAPK. We have previously demonstrated that temporal induction of Raf in the epidermis of K14-Raf:ER transgenic mice results in epidermal hyperplasia resembling squamous cell carcinoma and psoriasis. It has been demonstrated that epidermal Stat3 activation is required for psoriasis development, since keratinocyte-specific Stat3 activation in a mouse model elicits a psoriasis-like phenotype, which is reversed by inhibition of Stat3 signaling. Objective The aim of this study was whether Stat3 signaling is involved in Raf-MAPK-dependent epidermal hyperplasia. Methods K14-Raf:ER transgenic mice, in which the 4-hydroxytamoxifen (4OHT)-responsive mutant estrogen receptor ligand binding domain-Raf fusion gene is expressed under control of the keratin 14 promoter, were mated with epidermis-specific Stat3 null mice (K5-Cre.Stat3flox/flox). K5-Cre.Stat3flox/flox mice were used to define the impact of Stat3 deficiency on Raf-induced epidermal hyperplasia. Results Over-expression of Raf by 4OHT treatment in K14-Raf:ER;K5-Cre.Stat3flox/flox mice greatly attenuated the epidermal hyperplasia and dermal cell infiltrates compared with K14-Raf:ER;K5-Cre.Stat3flox/WT mice. Also, up-regulation of psoriasis-associated cytokine profiles, including VEGF, was inhibited in the skin from K14-Raf:ER;K5-Cre.Stat3flox/flox mice following 4OHT treatment. Conclusion These results clearly indicate that Raf-MAPK-dependent psoriatic-like epidermal hyperplasia requires Stat3 signaling in keratinocytes." @default.
• W2088631936 created "2016-06-24" @default.
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• W2088631936 date "2013-11-01" @default.
• W2088631936 modified "2023-09-27" @default.
• W2088631936 title "Epidermal hyperplasia induced by Raf-MAPK signaling requires Stat3 activation" @default.
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• W2088631936 doi "https://doi.org/10.1016/j.jdermsci.2013.06.007" @default.
• W2088631936 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23870655" @default.
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