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Phosphatidyl serine exposure during apoptosis precedes release of cytochrome c and decrease in mitochondrial transmembrane potential
Author(s) -
Denecker Geertrui,
Dooms Hans,
Van Loo Geert,
Vercammen Dominique,
Grooten Johan,
Fiers Walter,
Declercq Wim,
Vandenabeele Peter
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(99)01702-0
Subject(s) - cytochrome c , staurosporine , apoptosis , mitochondrion , mitochondrial apoptosis induced channel , microbiology and biotechnology , membrane potential , chemistry , programmed cell death , transmembrane protein , caspase , biology , biochemistry , signal transduction , protein kinase c , receptor
Time kinetics of phosphatidyl serine (PS) exposure were compared to other apoptotic parameters following different apoptotic stimuli. Our data indicate that anti‐Fas treatment of L929sAhFas cells results in rapid exposure of PS, which precedes decrease in mitochondrial transmembrane potential (Δ Ψ m ) and release of cytochrome c , indicating that PS exposure occurs independently of these mitochondrial events. Also during TNF‐, etoposide‐ or staurosporine‐mediated apoptosis in PC60 RI/RII cells, PS‐positive cells were observed before they had a decreased Δ Ψ m . However, during growth factor depletion‐induced death of 32D cells, both phenomena seemed to occur at the same time.