PMID- 12929750
OWN - NLM
STAT- MEDLINE
DCOM- 20040413
LR  - 20190818
IS  - 0031-8655 (Print)
IS  - 0031-8655 (Linking)
VI  - 78
IP  - 1
DP  - 2003 Jul
TI  - Ultraviolet A radiation induces rapid apoptosis of human leukemia cells by Fas 
      ligand-independent activation of the Fas death pathways.
PG  - 61-7
AB  - 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.
FAU - Zhuang, Shougang
AU  - Zhuang S
AD  - Wellman Laboratories of Photomedicine, Massachusetts General Hospital, Harvard 
      Medical School, Boston, MA 02114, USA.
FAU - Kochevar, Irene E
AU  - Kochevar IE
LA  - eng
GR  - GM30755/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Photochem Photobiol
JT  - Photochemistry and photobiology
JID - 0376425
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (Carrier Proteins)
RN  - 0 (FADD protein, human)
RN  - 0 (FASLG protein, human)
RN  - 0 (Fas Ligand Protein)
RN  - 0 (Fas-Associated Death Domain Protein)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (fas Receptor)
RN  - EC 3.4.22.- (CASP3 protein, human)
RN  - EC 3.4.22.- (CASP8 protein, human)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.22.- (Caspase 8)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - *Adaptor Proteins, Signal Transducing
MH  - *Apoptosis
MH  - Carrier Proteins/metabolism
MH  - Caspase 3
MH  - Caspase 8
MH  - Caspases/metabolism
MH  - Enzyme Activation
MH  - Fas Ligand Protein
MH  - Fas-Associated Death Domain Protein
MH  - HL-60 Cells
MH  - Humans
MH  - Leukemia/*metabolism/pathology
MH  - Membrane Glycoproteins/metabolism/physiology
MH  - Signal Transduction
MH  - *Ultraviolet Rays
MH  - Up-Regulation
MH  - fas Receptor/*metabolism
EDAT- 2003/08/22 05:00
MHDA- 2004/04/14 05:00
CRDT- 2003/08/22 05:00
PHST- 2003/08/22 05:00 [pubmed]
PHST- 2004/04/14 05:00 [medline]
PHST- 2003/08/22 05:00 [entrez]
AID - 10.1562/0031-8655(2003)078<0061:uarira>2.0.co;2 [doi]
PST - ppublish
SO  - Photochem Photobiol. 2003 Jul;78(1):61-7. doi: 
      10.1562/0031-8655(2003)078<0061:uarira>2.0.co;2.