[Effect of anoxic preconditioning on protein kinase C activity in neonatal rat cardiomyocytes].
In a model of anoxia/reoxygenation (A/R) of cultured rat cardiomyocytes, protection of cellular damage, activation of protein kinase C (PKC) and PKC-mediated protein phosphorylation by anoxic preconditioning (APC) can be demonstrated as shown by the increase of cell viability, attenuation of formation of lipid peroxides (MDA) and lowering of the leakage of lactate dehydrogenase (LDH) and protein from cells. The results also show that transient anoxia mimicked the outcomes of activation of PKC as shown by increased incorporation of 32P, especially in the 66 kD and 31 kD protein fractions. Preincubation of cardiomyocytes with H7 (an inhibitor of PKC) completely abolished these protective effects of transient anoxia. Protein phosphatase inhibitor OA mimicked the protective effects of A/R, while protein phosphatase activator BDM induced a complete abolishment. In short, we conclude that the protective effect of APC is medicated by activation of PKC.
Liu
X H
XH
Institute of Cardiovascular Research, Beijing Medical University.
Pang
Y Z
YZ
Tang
C S
CS
Su
J Y
JY
D000818:Animals; D000831:Animals, Newborn; D015687:Cell Hypoxia; D002478:Cells, Cultured; D019157:Ischemic Preconditioning, Myocardial; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D009206:Myocardium / Q000166:cytology / Q000201:enzymology*; D011493:Protein Kinase C / Q000378:metabolism*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar
D011493:Protein Kinase C