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Isoform-specific induction of PKC-epsilon by high glucose protects heart-derived H9c2 cells against hypoxic injury.

Authors
Kim, MH; Jung, YS; Moon, CH; Jeong, EM; Lee, SH; Baik, EJ; Moon, CK
Citation
Biochemical and biophysical research communications, 309(1):1-6, 2003
Journal Title
Biochemical and biophysical research communications
ISSN
0006-291X1090-2104
Abstract
We investigated which PKC isoforms are involved in high glucose-induced protection against hypoxic injury. Treatment for 48 h with high glucose (22 mM) markedly increased the expression of PKC- epsilon in the particulate fraction (213+/-22.1% of the control) but had no effect on other types of PKC isoforms, suggesting that the high glucose-induced increase in PKC expression is isoform-specific. The mRNA level for PKC- epsilon was also substantially increased, reaching its peak after 4h of high glucose treatment. The high glucose increased PKC-epsilon activity in the particulate fraction up to 183+/-32.2% of the control. During hypoxia, the amount of PKC-epsilon in the particulate fraction was remarkably diminished in the low glucose-treated cells, but remained at a higher level in high glucose-treated cells. The treatment with epsilon V1-2 (10 microM), a specific inhibitor of PKC epsilon, abolished the protective effect of high glucose against hypoxia. These results suggest that isoform-specific induction of PKC-epsilon is involved in high glucose-induced protection against hypoxic injury in heart-derived H9c2 cells.
MeSH terms
AnimalsAnoxia*Blotting, WesternCell DeathGlucose/metabolism*Myocardium/metabolismProtein IsoformsProtein Kinase C/chemistry*Protein Kinase C/metabolism*Protein Kinase C-epsilonRNA, Messenger/metabolismRatsTime FactorsTranscription, Genetic
PMID
12943654
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
AJOU Authors
정, 이숙문, 창현정, 의명이, 수환백, 은주
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