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Aspirin induces apoptosis through mitochondrial cytochrome c release
Author(s) -
Piqué Maria,
Barragán Montserrat,
Dalmau Mireia,
Bellosillo Beatriz,
Pons Gabriel,
Gil Joan
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)01922-0
Subject(s) - cytochrome c , apoptosis , caspase , jurkat cells , mitochondrial apoptosis induced channel , mitochondrion , microbiology and biotechnology , apoptosome , aspirin , chemistry , intrinsic apoptosis , inner mitochondrial membrane , programmed cell death , pharmacology , biology , biochemistry , immunology , t cell , immune system
Aspirin and other non‐steroidal anti‐inflammatory drugs induce apoptosis in many cell types. Although the involvement of caspases has been demonstrated, the mechanism leading to caspase activation remains unknown. We have studied the role of the mitochondrial pathway in aspirin‐induced apoptosis. The apoptotic effect of aspirin was analyzed in different cell lines (Jurkat, MOLT‐4, Raji and HL‐60) showing induction of mitochondrial cytochrome c release and caspases 9, 3 and 8 processing. Furthermore, early aspirin‐induced cytochrome c release was not affected by the caspase inhibitor Z‐VAD·fmk and preceded loss of mitochondrial membrane potential. Therefore, aspirin‐induced apoptosis involves caspase activation through cytochrome c release.