All-trans Retinoic Acid On Ultraviolet Induced Into The Molecular Mechanism Of Fiber Cells In The Influence Of The Mapk Pathway

Photoageing is caused by the effects of frequent and cumulatively prolonged sun exposure, specifically UVB and UVA radiation. Large, double-blind, vehicle-controlled studies have provided incontrovertible evidence that topical all-trans Retinoic Acid(at-RA) can improve photoaged skin. But the mechanism of its action is unclear.We employed an in-vitro model of photoageing developed by UVA irradiation on cultured human fibroblas The changes in cell proliferation and MAPK signal transductio(?) pathway induced by UVA were observed. Our results showed that at-RA stimulated cell proliferation; UVA exerted antiprolifer (?)tive effect, but the capability of fibroblast to proliferate was increased with at-RA pretreatment.The expression of c-Jun and c-H-ras pr(?)tein were significantly induced by UVA. at-RA induced their expression weakly. at-RA substantially reduced the elevated expre; sion of c-Jun and c-H-ras protein caused by UVA.C-Jun and c-H-ras mRNA levels were determined by Northern blot. Consistent with immunohistorical analysis, c-H-ras mRNA in cultured fibroblast were stimulated by UVA radiation and at-RA separately, at-RA reduced UVA-induced c-H-ras mRNA. C-Jun mRNA was markedly induced by UVA irradiation, but its level did not altered while treated with at-RA.According to our result, we proposed that (1)UVA exposure had the similar effect on photoageing compared with UVB radiation. UVA reaction involved the activation of MAP k(?)nases ERK, JNK and P38. Ras served an important role both in ERK and JNK pathway. Phosphoralation of c-Jun would lead to the activation of AP-1, ans ultimately causing photoageing. (2)The prevention of photoageing of at-RA(acting through nuclear retinoid receptors) may be connected with its action to inhibit induction of c-Jun protein by UVA irradiation and action to activate c-H-ras protein and mRNA .