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1 July 2003 Ultraviolet A Radiation Induces Rapid Apoptosis of Human Leukemia Cells by Fas Ligand–Independent Activation of the Fas Death Pathway
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Abstract

Endogenous cellular chromophores absorb ultraviolet A radiation (UVA, 290–320 nm), the major UV component of terrestrial solar radiation, leading to the formation of reactive oxidizing species that initiate apoptosis, gene expression and mutagenesis. UVA-induced apoptosis of T helper cells is believed to underlie the UVA phototherapy for atopic dermatitis and other T cell–mediated inflammatory skin diseases. We have evaluated the involvement of the Fas–Fas ligand (FasL) pathway in rapid UVA-induced apoptosis in human leukemia HL-60 cells. UVA-induced apoptosis was not inhibited by pretreatment with a neutralizing anti-Fas antibody, although the same UVA treatment initiated cleavage of caspase-8 and subsequent processing of Bid and caspase-3–like proteases. Inhibition of caspase-8 by Lle-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone completely blocked caspase-3 cleavage and apoptosis in UVA-treated cells, suggesting that apoptosis was initiated by the Fas pathway. This inference was supported by demonstrating that immunoprecipitates obtained from UVA-treated cells using anti-Fas antibody contained caspase-8 and Fas-associating protein with death domain (FADD). In addition, Fas clustering in response to UVA treatment was observed by immunofluorescence microscopy. These data support a mechanism for rapid, UVA-induced apoptosis in HL-60 cells involving initial formation of the Fas–FADD–caspase-8 death complex in an FasL-independent manner.

Shougang Zhuang and Irene E. Kochevar "Ultraviolet A Radiation Induces Rapid Apoptosis of Human Leukemia Cells by Fas Ligand–Independent Activation of the Fas Death Pathway," Photochemistry and Photobiology 78(1), 61-67, (1 July 2003). https://doi.org/10.1562/0031-8655(2003)078<0061:UARIRA>2.0.CO;2
Received: 17 December 2002; Accepted: 1 April 2003; Published: 1 July 2003
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