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A Almony, S Garg, R Sanchez, Q Chu, AA Sadun, TT Lam; Protein KinaseC(PKC) and Cell Survival After Retinal Ischemic-Reperfusion Injury . Invest. Ophthalmol. Vis. Sci. 2002;43(13):773.
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Purpose: To probe the role of protein kinase C (PKC) in inner retinal tissue response to retinal ischemic-reperfusion injury in rats.Method: Elevated intraocular pressure was maintained for 60 minutes in anesthetized male albino Lewis rats by cannulating the anterior chamber with a needle connected to a saline column that delivered a pressure of 110 mmHg. PMA (PKC activator; 10µM), Go 7874 (PKC Inhibitor; 20nM), or vehicle (0.5% DMSO in saline) was infused through the cannula during the ischemic period. Reperfusion was established immediately after the 60-minute ischemic period. All animals were euthanized after 7 days and whole-mount flat preparations of retinas were made. The nuclei in the retinal ganglion cell layer (RGCL) were counted after cresyl violet staining. Results: Compared to the vehicle-treated retinas, PMA-treated retinas had a significantly higher number of nuclei in the RGCL (P<0.001; n=8), whereas Go7874-treated retinas had a significantly lower number (P<0.001; n=7).Conclusion: PKC activation is neuroprotective and PKC may have a pivotal role in mediating neuronal cell survival after retinal ischemia-reperfusion injury.
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