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Role for PKC-epsilon in neuronal death induced by oxidative stress.

Authors
Jung, YS; Ryu, BR; Lee, BK; Mook-Jung, I; Kim, SU; Lee, SH; Baik, EJ; Moon, CH
Citation
Biochemical and biophysical research communications, 320(3):789-794, 2004
Journal Title
Biochemical and biophysical research communications
ISSN
0006-291X1090-2104
Abstract
We investigated which isoforms of PKCs can be modulated and what their roles are during l-buthionine-S,R-sulfoximine (BSO)-induced neuronal death. We observed the isoform specific translocation of PKC-epsilon from the soluble fraction to the particulate in cortical neurons treated with 10 mM BSO. The translocation of PKC-epsilon by BSO was blocked by antioxidant trolox, suggesting the PKC-epsilon as a downstream of reactive oxygen species (ROS) elevated by BSO. Trolox inhibited the ROS elevation and the neuronal death in BSO-treated cortical cells. The BSO-induced neuronal death was remarkably inhibited by both the pharmacological inhibition of PKC-epsilon with epsilonV1-2 and the functional blockade for PKC-epsilon through overexpression of PKC-epsilon V1 region, suggesting the detrimental role of PKC-epsilon. These results suggest that PKC-epsilon is the major PKC isoform involved in the pathways triggered by ROS, leading to neuronal death in BSO-treated cortical neurons.
MeSH terms
AnimalsApoptosis/physiologyButhionine Sulfoximine/*pharmacologyCells, CulturedDose-Response Relationship, DrugEnzyme Activation/drug effectsGlutathione/*metabolismIsoenzymes/chemistry/metabolismMiceNeocortex/cytology/drug effects/embryology/*metabolismNeurons/cytology/drug effects/*physiologyOxidative Stress/*physiologyPeptide Fragments/pharmacologyProtein Kinase C/antagonists & inhibitors/chemistry/*metabolism/pharmacologyProtein Kinase C-epsilonReactive Oxygen Species/*metabolismStructure-Activity Relationship
DOI
10.1016/j.bbrc.2004.05.217
PMID
15240117
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
Journal Papers > School of Medicine / Graduate School of Medicine > Neurology
AJOU Authors
정, 이숙김, 승업이, 수환백, 은주문, 창현
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