Molecular Mechanism of Ultraviolet-Induced Keratinocyte Apoptosis

摘要: This article reviews advances in the study of molecular mechanisms for ultraviolet (UV)-induced keratinocyte apoptosis, with particular reference to cytokines tumor necrosis factor-alpha (TNF-alpha) and Fas ligand (FasL). TNF-alpha FasL induce their respective receptors then activate caspase enzymes that are critically involved apoptotic process. activation is further amplified by intracellular mitochondria-associated mechanisms. Using gene-targeted knockout mice lacking either TNF-Rp55 or TNF-Rp75, we have shown plays an important role UV-induced apoptosis via TNF-Rp55. shares homology contains death domain. UV seems directly stimulate cross-linking Fas, resulting engagement machinery. Fas-associated domain protein (FADD) acts as adapter both death-inducing cascades responsible downstream signal transduction recruiting caspases. Moreover, signaling p53 contributes induction regulating Bcl-2 family expression increasing surface expression. In addition there numerous inhibitory molecules play a restricting pathway. Thus, ultimate determination whether not cell undergoes after radiation based on balance between agonist antagonist pathways.