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Phosphatidylserine exposure in Fas type I cells is mitochondria‐dependent
Author(s) -
Uthaisang Wanlaya,
Nutt Leta K,
Orrenius Sten,
Fadeel Bengt
Publication year - 2003
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(03)00508-8
Subject(s) - phosphatidylserine , mitochondrion , apoptosis , microbiology and biotechnology , caspase , dna fragmentation , fas receptor , programmed cell death , effector , biology , chemistry , membrane , biochemistry , phospholipid
Previous studies have demonstrated that Fas‐triggered activation of effector caspases and subsequent nuclear apoptosis either is mitochondria‐independent (type I cells) or relies on mitochondrial amplification of the initial stimulus (type II cells). We show herein that Bcl‐2 overexpression in a prototypic type I cell line (SKW6.4) promotes mitochondrial generation of ATP and blocks Fas‐triggered plasma membrane externalization of phosphatidylserine (PS). Moreover, overexpression of Bcl‐2 attenuates macrophage engulfment of Fas‐triggered cells. Fas‐mediated DNA fragmentation, on the other hand, remains unaffected in SKW6.4‐ bcl‐2 cells. These studies thus demonstrate that PS externalization and clearance of cell corpses are mitochondria‐dependent events, and show that these events can be dissociated from other features of the apoptotic program, in Fas type I cells.