Isoform-specific induction of PKC-epsilon by high glucose protects heart-derived H9c2 cells against hypoxic injury.
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.
Kim
Min Hwa
MH
College of Pharmacy, Seoul National University, Republic of Korea.
Jung
Yi-Sook
YS
Moon
Chang-Hyun
CH
Jeong
Euy-Myoung
EM
Lee
Soo Hwan
SH
Baik
Eun Joo
EJ
Moon
Chang-Kiu
CK
D000818:Animals; D015153:Blotting, Western; D016923:Cell Death; D005947:Glucose / Q000378:metabolism*; D000860:Hypoxia; D009206:Myocardium / Q000378:metabolism; D020033:Protein Isoforms; D011493:Protein Kinase C / Q000737:chemistry* / Q000378:metabolism*; D051744:Protein Kinase C-epsilon; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D013997:Time Factors; D014158:Transcription, Genetic
D020033:Protein Isoforms; D012333:RNA, Messenger; C497257:Prkce protein, rat; D011493:Protein Kinase C; D051744:Protein Kinase C-epsilon; D005947:Glucose