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Phosphatidylserine induces apoptosis in CHO cells without mitochondrial dysfunction in a manner dependent on caspases other than caspases‐1, ‐3, ‐8 and ‐9
Author(s) -
Miyato Yasuyuki,
Ibuki Yuko,
Ohyama Harumi,
Yamada Takeshi,
Goto Rensuke
Publication year - 2001
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(01)02771-5
Subject(s) - phosphatidylserine , apoptosis , cytochrome c , caspase , camptothecin , chinese hamster ovary cell , microbiology and biotechnology , mitochondrion , caspase 9 , mitochondrial apoptosis induced channel , biology , intrinsic apoptosis , caspase 3 , membrane potential , chemistry , programmed cell death , biochemistry , phospholipid , receptor , membrane
Treatment of Chinese hamster ovary K1 cells with phosphatidylserine (PS) caused typical apoptosis with distinct morphological and biochemical features in a dose‐ and time‐dependent manner. However, unlike camptothecin‐induced apoptosis, changes in mitochondrial transmembrane potential were not observed. In addition, cytochrome c release did not occur in PS‐induced apoptosis. A pan caspase inhibitor, Z‐VAD, significantly inhibited the apoptosis, but inhibitors of caspase‐1, ‐3, ‐8 and ‐9 did not. Activities of caspase‐1, ‐3, ‐8 and ‐9 were increased by treatment of the cells with camptothecin, but not with PS. These results suggest that PS‐induced apoptosis occurs without the collapse of mitochondrial transmembrane potential and without the release of cytochrome c , in a manner independent of caspase‐1, ‐3, ‐8 and ‐9.