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Depolarisation of the plasma membrane in the arsenic trioxide (As 2 O 3 )‐and anti‐CD95‐induced apoptosis in myeloid cells
Author(s) -
Nolte Florian,
Friedrich Oliver,
Rojewski Markus,
Fink Rainer H.A.,
Schrezenmeier Hubert,
Körper Sixten
Publication year - 2004
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/j.febslet.2004.10.075
Subject(s) - depolarization , arsenic trioxide , apoptosis , chemistry , fas receptor , membrane , membrane potential , biophysics , cell , microbiology and biotechnology , programmed cell death , biology , biochemistry
Depolarisation of the plasma membrane has been shown to be actively regulated during lymphocyte‐apoptosis. Here, we present data about anti‐Fas and As 2 O 3 induced depolarisation of myeloid U‐937 cells. Anti‐Fas but not As 2 O 3 ‐induced depolarisation was significantly dependent on caspase‐activation. Na + ‐fluxes contributed to the depolarisation in early stages of As 2 O 3 ‐induced apoptosis, whereas the membrane potential in late stages depended on Cl − ‐fluxes. Cl − ‐channels also played an important role in the induction of cell shrinkage in As 2 O 3 ‐induced apoptosis. However, none of these ions contributed significantly to anti‐Fas induced depolarisation. This indicates the existence of different mechanisms for apoptotic plasma membrane depolarisation within one cell type.