November 1996
Volume 37, Issue 12
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Articles  |   November 1996
Hyperthermia and hypoxia increase tolerance of retinal ganglion cells to anoxia and excitotoxicity.
Author Affiliations
  • J Caprioli
    Yale University School of Medicine, Department of Ophthalmology and Visual Science, New Haven, Connecticut, USA.
  • S Kitano
    Yale University School of Medicine, Department of Ophthalmology and Visual Science, New Haven, Connecticut, USA.
  • J E Morgan
    Yale University School of Medicine, Department of Ophthalmology and Visual Science, New Haven, Connecticut, USA.
Investigative Ophthalmology & Visual Science November 1996, Vol.37, 2376-2381. doi:
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    • Get Citation

      J Caprioli, S Kitano, J E Morgan; Hyperthermia and hypoxia increase tolerance of retinal ganglion cells to anoxia and excitotoxicity.. Invest. Ophthalmol. Vis. Sci. 1996;37(12):2376-2381.

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

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Abstract

PURPOSE: Knowledge of the mechanisms by which retinal ganglion cells are damaged may provide information required to develop novel treatments for diseases that cause retinal ganglion cell death. The authors investigated whether the expression of the 72-kDa heat shock protein in cultured rat retinal ganglion cells increases tolerance to hypoxic and excitotoxic injury. METHODS: Hyperthermia (42 degrees C for 1 hour) and sublethal hypoxia (9% O2 for 6 hours) were used to induce synthesis of the 72-kDa heat shock protein in cultured rat retinal ganglion cells and cultured retinal Müller cells. Induction of the 72-kDa heat shock protein was detected with immunocytochemical and immunoblot techniques. Survival of cultured retinal ganglion cells after exposure to anoxia (< 1% O2 for 6 hours) and glutamate (200 microns for 6 hours) was measured and compared to control cultures stressed previously by hyperthermia or sublethal hypoxia. The effect of quercetin, a blocker of heat shock protein synthesis, was evaluated in parallel experiments. RESULTS: Heat shock protein immunoreactivity was expressed in cultured retinal ganglion cells and Müller cells after hyperthermia and sublethal hypoxia. The mean (+/- standard deviation) retinal ganglion cell survival rates after exposure to anoxia (expressed as a percentage of untreated control cultures) in cells pretreated with sublethal hypoxia (83% +/- 17%) and hyperthermia (82% +/- 19%) were significantly greater than for cells that had no pretreatment (50% +/- 18%, P < 0.001). The mean (+/-standard deviation) retinal ganglion cell survival rate after exposure to glutamate in cells pretreated with sublethal hypoxia (82% +/- 19%) and hyperthermia (86% +/- 17%) were significantly greater than for cells that had no pretreatment (56% +/- 17%, P < 0.001). Inhibition of heat shock protein synthesis with quercetin abolished the protective effects of sublethal hypoxia and hyperthermia on cell survival after anoxia and glutamate exposure. CONCLUSIONS: The neuroprotective effect of hyperthermia and sublethal hypoxia suggests that heat shock proteins confer protection against ischemic and excitotoxic retinal ganglion cell death.

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