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ULTRAVIOLET B IRRADIATION MODULATES SUSCEPTIBILITY TO TUMOUR NECROSIS FACTOR‐α‐INDUCED APOPTOSIS VIA INDUCTION OF DEATH RECEPTORS IN MURINE FIBROBLASTS
Author(s) -
Kimura Hirokazu,
Minakami Hisanori
Publication year - 2001
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1006/cbir.2001.0805
Subject(s) - apoptosis , tumor necrosis factor alpha , programmed cell death , fas receptor , uvb induced apoptosis , dna fragmentation , microbiology and biotechnology , receptor , fibroblast , fas ligand , biology , cancer research , inducer , necrosis , cell culture , chemistry , immunology , caspase , biochemistry , gene , genetics
Ultraviolet B (UVB) irradiation causes cell death by apoptosis in murine fibroblast cells. Tumor necrosis factor‐α (TNF‐α) is also a well known inducer of apoptosis, although the physiological significance of this activity is poorly understood. We investigated the effects of pretreatment with UVB (312nm) on TNF‐α‐induced apoptosis in murine fibroblast cells. UVB enhanced susceptibility to cell death by TNF‐α in a dose‐dependent manner. UVB but not TNF‐α induced the expression of TNF receptor type‐1 (TNFR‐1) and type‐2 (TNFR‐2) in a dose‐dependent manner. Expression of Fas (CD95) and Fas‐ligand (Fas‐L), and significant DNA fragmentation were observed in the cells that died. These results suggest that UVB irradiation modulates susceptibility to TNF‐α‐induced apoptosis through the induction of TNFRs, Fas, and Fas‐L in murine fibroblasts.