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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.
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Full text: Available 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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Full text: Available 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