Premium
Possible contribution of apoptosis‐inducing factor (AIF) and reactive oxygen species (ROS) to UVB‐induced caspase‐independent cell death in the T cell line Jurkat
Author(s) -
Murahashi Hideaki,
Azuma Hiroshi,
Zamzami Naoufal,
Furuya Koji,
Ikebuchi Kenji,
Yamaguchi Miki,
Yamada Yoshiko,
Sato Norihiro,
Fujihara Mitsuhiro,
Kroemer Guido,
Ikeda Hisami
Publication year - 2003
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0702335
Subject(s) - jurkat cells , apoptosis inducing factor , apoptosis , biology , programmed cell death , dna fragmentation , microbiology and biotechnology , phosphatidylserine , reactive oxygen species , caspase , fragmentation (computing) , chromosomal translocation , t cell , immunology , biochemistry , phospholipid , ecology , immune system , membrane , gene
We analyzed the mechanism of UVB‐induced cell death using the Jurkat T cell line. Apoptosis was assessed by measuring phosphatidylserine (PS) externalization, caspase activity, the decrease in mitochondrial membrane potential (ΔΨm), nucleosomal DNA fragmentation, and morphological changes such as chromatin condensation. The mitochondrio‐nuclear translocation of apoptosis‐inducing factor (AIF) was evaluated by confocal laser microscopy. The cell death pattern of UVB‐irradiated cells was similar to the Fas‐induced cell death pattern. However, zVAD‐fmk inhibited the nucleosomal fragmentation of DNA but not the externalization of PS, decrease in ΔΨm, or mitochondrio‐nuclear translocation of AIF. N‐acetyl L‐cysteine significantly inhibited the translocation of AIF induced by UVB. These results suggested that caspase‐dependent and ‐independent pathways were involved in UVB‐induced cell death in Jurkat cells, and the mitochondrio‐nuclear translocation of AIF was associated with the latter pathway. In addition, reactive oxygen species generated by UVB might be involved in inducing the mitochondrio‐nuclear translocation of AIF.