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Abstract
UV irradiation acts as a broad activator of cell surface growth factor and cytokine
receptors. This ligand-independent receptor activation induces multiple downstream
signaling pathways that regulate expression of multiple genes. These signaling pathways
converge to stimulate transcription factor AP-1. Among genes whose expression is regulated
by AP-1 are several matrix-metalloproteinase (MMP) family members and type I procollagen.
UV-enhanced matrix degradation is accompanied with decreased collagen production mediated
not only by activation of AP-1, but also by inhibition of transforming growth factor
(TGF)-beta signaling. Several alterations to skin connective tissue that occur during
aging are mediated by mechanisms that are similar to those that occur in response
to UV irradiation. Thus, skin aging is associated with increased AP-1 activity, increased
MMP expression, impaired TGF-beta signaling, enhanced collagen degradation, and decreased
collagen synthesis. Knowledge gained from examining molecular responses of human skin
to UV irradiation provides not only a framework for understanding mechanisms involved
in skin aging, but also may help in development of new clinical strategies to impede
chronological and UV-induced skin aging.