April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
CaMKII Inhibitor Protects Retinal Ganglion Cells in the Ischemia-Reperfusion Model
Author Affiliations & Notes
  • W. Fan
    Anatomical Sciences & Neurobiology,
    Univ of Louisville Sch of Med, Louisville, Kentucky
  • N. G. F. Cooper
    Anatomical Sciences & Neurobiology, Ophthalmology & Visual Sciences,
    Univ of Louisville Sch of Med, Louisville, Kentucky
  • Footnotes
    Commercial Relationships  W. Fan, None; N.G.F. Cooper, None.
  • Footnotes
    Support  NIH grants: P20RR016481; R01EY017594; 1P30ES014443
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 129. doi:
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      W. Fan, N. G. F. Cooper; CaMKII Inhibitor Protects Retinal Ganglion Cells in the Ischemia-Reperfusion Model. Invest. Ophthalmol. Vis. Sci. 2009;50(13):129.

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

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Abstract

Purpose: : Our laboratory is the first to show the presence in the retinal ganglion cells (RGCs) of a nuclear isoform of CaMKII-alpha, CaMKII-alphaB, an alternative transcript expressed in response to glutamate or NMDA stimulation. While cytoplasmic CaMKII-alpha is most likely involved the cell death pathways, the nuclear CaMKII-alphaB mediates a survival response in RGCs. Balance of cytoplasmic and nuclear pathways may dictate the fate of RGCs. The purpose of the present study is to determine if there is any involvement of CaMKII-alpha in retinal ischemia.

Methods: : Retinal ischemia was induced by transiently elevating intraocular pressure to 110 mmHg for 60 minutes in Long Evan rats, with or without the autocamtide-2-related inhibitory peptide (AIP, a specific CaMKII inhibitor) injected intravitreally two hours before inducing ischemia. A sham-procedure served as a control. Following reperfusion for various periods of time, cell death was assessed on retinal flat mounts with the aid of AnnexinV conjugated to AlexaFluor. Expression and phosphorylation of CaMKII-alpha was determined by real time PCR and western blots, respectively.

Results: : Twenty-four hours after reperfusion, apoptotic RGCs were detected in ischemic retinas. The cell death was significantly blocked with AIP. Correspondingly, phophorylated CaMKII-alpha was detected in cytoplasmic protein in ischemia at an early time point and AIP inhibited the phosphorylation. Expression of nuclear CaMKII-alphaB increased with time after reperfusion and peaked at 24 hours.

Conclusions: : These data implicate the involvement of CaMKII-alpha in retinal ischemia, and demonstrate that CaMKII inhibitor protects RGCs from this injury. CaMKII-alpha may be a potential target for neuroprotection in vision disorders induced by retinal ischemia.

Keywords: ganglion cells • ischemia • cell survival 
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