Determination of conventional protein kinase C isoforms involved in high intraocular pressure-induced retinal ischemic preconditioning of rats.

Evidence indicates that conventional protein kinase C (cPKC) plays a pivotal role in the development of retinal ischemic preconditioning (IPC). In this study, the effect of high intraocular pressure (IOP)-induced retinal IPC on cPKC isoform-specific membrane translocation and protein expression were observed. We found that cPKCgamma membrane translocation increased significantly at the early stage (20min-1h), while the protein expression levels of cPKCalpha and gamma were markedly elevated in the delayed retinal IPC (12-168h) of rats. The increased protein expressions of cPKCalpha at 72h and cPKCgamma at 24h after IPC were further confirmed by immunofluorescence staining. In addition, we found that cPKCgamma co-localized with retinal ganglion cell (RGC)-specific marker, neurofilaments heavy chain (NF-H) by using double immunofluorescence labeling. These results suggest that increased cPKCgamma membrane translocation and up-regulated protein expressions of cPKCalpha and gamma are involved in the development of high IOP-induced rat retinal IPC.