UVC inhibits collagen biosynthesis through up-regulation of NF-κB p65 signaling in cultured fibroblasts.

The effects of UVC on collagen biosynthesis, prolidase activity, expression of α₂β₁ integrin, IGF-I receptor, FAK, MAP-kinases (ERK1 and ERK2) and the transcription factor NF-κB p65 were evaluated in human dermal fibroblasts. Confluent fibroblasts were treated with UVC light at a rates of 30 and 60 J/m(2). It was found that UVC-dependent decrease in collagen biosynthesis was not accompanied by parallel decrease in prolidase activity and expression. Since insulin-like growth factor receptor (IGF-IR) and α₂β₁ integrin signaling are the most potent regulators of collagen biosynthesis, the effect of UVC on IGF-IR and α₂β₁ integrin receptor expressions were evaluated. It was found that the exposure of the cells to UVC contributed to decrease in α₂β₁ integrin receptor and FAK expression and to an increase in IGF-IR and pERK1, pERK2 expressions. It was accompanied by an increase in the expression of NF-κB p65, the known inhibitor of collagen gene expression. The data suggest that UVC-dependent decrease of collagen biosynthesis in cultured human skin fibroblasts results from decrease in α₂β₁ integrin receptor signaling and activation of NF-κB p65, that is responsible for down-regulation of collagen gene expression.