Glutathione Depletion by L-Buthionine-S,R-Sulfoximine Induces Apoptosis of Cardiomyocytes through Activation of PKC-delta
Biomolecules & Therapeutics
;
: 358-363, 2013.
Article
in English
| WPRIM
| ID: wpr-108277
ABSTRACT
In the present study, we investigated the effect of intracellular glutathione (GSH) depletion in heart-derived H9c2 cells and its mechanism. L-buthionine-S,R-sulfoximine (BSO) induced the depletion of cellular GSH, and BSO-induced reactive oxygen species (ROS) production was inhibited by glutathione monoethyl ester (GME). Additionally, GME inhibited BSO-induced caspase-3 activation, annexin V-positive cells, and annexin V-negative/propidium iodide (PI)-positive cells. Treatment with rottlerin completely blocked BSO-induced cell death and ROS generation. BSO-induced GSH depletion caused a translocation of PKC-delta from the cytosol to the membrane fraction, which was inhibited by treatment with GME. From these results, it is suggested that BSO-induced depletion of cellular GSH causes an activation of PKC-delta and, subsequently, generation of ROS, thereby inducing H9c2 cell death.
Full text:
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Index:
WPRIM (Western Pacific)
Main subject:
Cell Death
/
Reactive Oxygen Species
/
Apoptosis
/
Cytosol
/
Myocytes, Cardiac
/
Caspase 3
/
Glutathione
/
Membranes
Language:
English
Journal:
Biomolecules & Therapeutics
Year:
2013
Type:
Article
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