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The molecular determinants of sunburn cell formation
Author(s) -
Murphy G.,
Young A. R.,
Wulf H. C.,
Kulms D.,
Schwarz T.
Publication year - 2001
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1034/j.1600-0625.2001.010003155.x
Subject(s) - apoptosis , sunburn , programmed cell death , fas receptor , microbiology and biotechnology , epidermis (zoology) , receptor , oxidative stress , cancer research , cell , dna damage , biology , chemistry , genetics , biochemistry , dna , medicine , dermatology , anatomy
Sunburn cell (SBC) formation in the epidermis is a characteristic consequence of ultraviolet radiation (UVR) exposure at doses around or above the minimum erythema dose. SBC have been identified morphologically and biologically as keratinocytes undergoing apoptosis. There is evidence that SBC formation is a protective mechanism to eliminate cells at risk of malignant transformation. The level of DNA photodamage is a major determinant of SBC induction by a process controlled by the tumor suppressor gene p53. However, extra‐nuclear events also contribute to SBC formation, such as the activation of death receptors including CD95/Fas. UVR triggers death receptors either by direct activation of these surface molecules or by inducing the release of their ligands such as CD95 ligand or tumor necrosis factor. Oxidative stress also appears to be involved, probably via mitochondrial pathways, resulting in the release of cytochrome C. Pathways which modify SBC formation are now extensively studied given the importance of apoptosis in eliminating irreparably damaged cells. A greater understanding of the mechanisms that induce and prevent UVR‐induced apoptosis will contribute to our understanding of mechanisms relevant in genomic integrity.