Changes in cPKC isoform-specific membrane translocation and protein expression in the brain of hypoxic preconditioned mice

Previous studies have shown that the level of total conventional protein kinase C (cPKC) membrane translocation (activation) was increased in the brain of hypoxic preconditioned mice. In order to find out which isoform of cPKC may participate in the development of cerebral hypoxic preconditioning (HPC), we used Western bolt and immunohistochemistry to observe the effects of repetitive hypoxic exposure (H1-H6, n = 6 for each group) on the level of cPKC isoform-specific protein expression and its membrane translocation in the cortex and hippocampus of mice. We found that the levels of cPKC betaII and gamma membrane translocation were increased significantly (p < 0.05 versus normoxic H0 group, n = 6) in response to repetitive hypoxic exposure (H1-H4) at an early phase of hypoxic preconditioning, but no significant changes of cPKC alpha and betaI membrane translocation were found during cPKC alpha, betaI, betaII and gamma protein expression both in hippocampus and cortex. In addition, an extensive subcellular redistribution of cPKC betaII and gamma was detected by immunohistochemistry staining in the cortex after repetitive hypoxic exposures (H3). However, a significant decrease in the expression of cPKC gamma protein (p < 0.05 versus H0 group) was found only in the cortex of delayed hypoxic preconditioned mice (H5-H6). These results suggest that the activation of cPKC betaII and gamma may be involved in the early phase of cerebral hypoxic preconditioning and the changes in cPKC gamma protein expression may participate in the development of the late phase of cerebral hypoxic preconditioning as well as selective vulnerability to hypoxia both in cortex and hippocampus.