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Yasushi Kitaoka, Yasunari Munemasa, Kaori Kojima, Yasuhiro Hayashi, Satoki Ueno; Involvement of Autophagy in Axonal Protection by Nicotinamide Mononucleotide Adenylyltransferase3 (Nmnat3) Overexpression Against High IOP-induced Optic Nerve Degeneration. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4678.
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To investigate the role of autophagy on axonal protective effect of Nmnat3 in high IOP-induced optic nerve degeneration.
Eight-week-old male Wistar rats were received the combination of injection of india ink and laser treatment to trabecular meshwork. Overexpression of Nmnat3 was performed with electroporation after intravitreal injection of DNA plasmid. The effects of Nmnat3 overexpression on axon were evaluated by electron microscopy (EM) as well as axon number counting 3 weeks after glaucoma induction. The expression of Nmnat3 and LC3 in optic nerve was examined by Western blot analysis and immunohistochemistry.
Immunohistochemistry showed that Nmnat3 and LC3 exist not only in the RGC but also in the optic nerve axon. Nmnat3 overexpression significantly ameliorated the axonal loss induced by high IOP. Western blot analysis showed that Nmnat3 overexpression significantly increased the level of LC3 protein in optic nerve compared to control plasmid injection. EM analysis revealed that there are recognizable autophagic vacuoles and degenerative changes in axon after glaucoma induction. In glaucoma eyes with Nmnat3 overexpression, autophagic vacuoles were also observed, but organization of microtubules was well preserved.
LC3 is found in both the RGC body and axon. Autophagy may be involved in axonal protection by Nmnat3 overexpression against high IOP-induced optic nerve degeneration.
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