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Y. Kitaoka, Y. Munemasa, J. Kuribayashi, Y. Hayashi, S. Ueno; Axonal Protection by Nicotinamide Mononucleotide Adenylyltransferase3 (Nmnat3) in TNF-Induced and High IOP-Induced Optic Nerve Degeneration. Invest. Ophthalmol. Vis. Sci. 2010;51(13):1082.
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To examine the role of Nmnat3 on axonal loss in TNF-induced and high IOP-induced optic nerve degeneration.
Eight-week-old male Wistar rats were divided into TNF-induced optic nerve degeneration groups and glaucoma groups. The TNF groups were received intravitreal injection of 10 ng TNF-α or PBS. The glaucoma induction was performed by combination of injection of india ink and laser treatment to trabecular meshwork. Overexpression of Nmnat3 on the retina was performed with electroporation after intravitreal injection of DNA plasmid. The effects of Nmnat3 overexpression on axonal loss were evaluated 2 weeks after intravitreal injection or 3 weeks after glaucoma induction. The expression of Nmnat3 in optic nerve was examined by Western blot analysis and immunohistochemistry.
Immunohistochemistry showed the substantial co-localization of Nmnat3 and neurofilament in the optic nerve. Western blot analysis and flatmounted retina demonstrated successful transfection of Nmnat3 DNA plasmid into the retinal ganglion cells. Axon number was significantly decreased in control EGFP-transfected eyes with TNF injection compared to PBS injection. Nmnat3 overexpression significantly ameliorated TNF-induced axonal loss. The axon number was significantly decreased in glaucoma compared to the sham control. Nmnat3 overexpression also ameliorated the axonal loss induced by high IOP.
Nmnat3 can exert axonal protection against TNF-induced and high IOP-induced optic nerve degeneration.
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