December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Protein KinaseC(PKC) and Cell Survival After Retinal Ischemic-Reperfusion Injury
Author Affiliations & Notes
  • A Almony
    Ophthalmology University of Southern California Keck School of Medicine/Doheny Eye Institute Los Angeles CA
  • S Garg
    Ophthalmology University of Southern California Keck School of Medicine/Doheny Eye Institute Los Angeles CA
  • R Sanchez
    Ophthalmology University of Southern California Keck School of Medicine/Doheny Eye Institute Los Angeles CA
  • Q Chu
    Ophthalmology University of Southern California Keck School of Medicine/Doheny Eye Institute Los Angeles CA
  • AA Sadun
    Ophthalmology University of Southern California Keck School of Medicine/Doheny Eye Institute Los Angeles CA
  • TT Lam
    Ophthalmology University of Southern California Keck School of Medicine/Doheny Eye Institute Los Angeles CA
  • Footnotes
    Commercial Relationships   A. Almony, None; S. Garg, None; R. Sanchez, None; Q. Chu, None; A.A. Sadun, None; T.T. Lam, None. Grant Identification: NIH Grant EY03040; RPB unrestricted grant
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 773. doi:
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    • Get Citation

      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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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : 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.

Keywords: 448 ischemia • 489 neuroprotection • 514 pharmacology 
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