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"FOREIGN", "hungarian" : false, "published" : true, "oldId" : 812, "snippet" : true }, "volume" : "174", "issue" : "3", "firstPage" : "533", "lastPage" : "541", "firstPageOrInternalIdForSort" : "533", "pageLength" : 9, "publishedYear" : 2016, "abstractText" : "BACKGROUND: Data indicate that in psoriasis abnormalities are already present in the non-lesional skin. TGFbeta, KGF together with fibronectin and alpha5beta1 integrin was suggested to play a crucial role in the pathogenesis of psoriasis by influencing inflammation and keratinocyte hyperproliferation. OBJECTIVES: To investigate the expression of KGF, FGFR2, fibronectin (FN) and EDA+ FN in healthy and non-lesional psoriatic skin and to study the effect of KGF on the regulation of FN and EDA+ FN production by fibroblasts. METHODS: Healthy, non-lesional psoriatic skin and lesional psoriatic skin were immmunostained for alpha5 integrin, KGF, FGFR2, EDA+ FN and STAT1. KGF treated cell cultures were analyzed for FN and EDA+ FN mRNA and protein by real-time RT-PCR and flow cytometry respectively. The four major downstream signaling of KGF was investigated by blocking experiments using MEK1, AKT1/2, STAT1 and STAT3 inhibitors. RESULTS: The expression of alpha5 integrin, EDA+ FN, KGF and its receptor FGFR2 is elevated in psoriatic non-lesional skin compared to healthy skin. KGF mildly induced EDA+ FN, but not FN expression in healthy fibroblasts through MAPK signaling. Fibroblasts express the FGFR2-IIIc. STAT1 negatively regulates both FN and EDA+ FN expressions in healthy fibroblasts and this regulation is compromised in fibroblasts derived from non-lesional psoriatic dermis. We detected active STAT1 in healthy and lesional skin, similar to a previous report, however, in the non-lesional skin STAT1 activation was absent in tissues far away from lesions. CONCLUSIONS: The production of FN, EDA+ FN by fibroblasts and the signaling of STAT1 is abnormally regulated in the psoriatic non-lesional skin. This article is protected by copyright. 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