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Y. Munemasa, Y. Kitaoka, R. Ohtani–Kaneko, Y. Hayashi, K. Kuribayashi, J. Kogo, H. Takeda, K. Hirata, S. Ueno; Activation of Erk by Endothelin–1 Induced Neurotoxicity in the Rat Retina . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2057.
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Endothelin–1 (ET–1) is a potent vasoconstrictor peptide produced by vascular endothelial cells. Previous reports have shown that intravitreal injection of ET–1 induced optic nerve head (ONH) ischemia. However, the detail mechanism of ET–1–induced neuronal damage is unclear. In this study, we examined the expression of phosphorylated ERK (p–ERK) in ET–1–induced neurotoxicity in the rat retina and optic nerve.
Two micro liter of 0.1 mM (total amount of 0.2 nmol) ET–1 was injected intravitreally into the eye. Activation of ERK was examined by Western blot analysis and its localization was detected by immunohistochemistry. Axonal degeneration of optic nerve was evaluated by Western blot analysis for neurofilament (NF) and phosphorylated neurofilament (p–NF) 7, 14, 21 and 28 days after the injection. Cell count of the RGCL and measurement of the IPL thickness were performed by HE staining of the retinal transverse sections 14 and 28 days after the injection.
Western blot analysis showed the increase of p–ERK in the retina and the optic nerve 1 day after the injection. Immunoreactivity of p–ERK was detected in the glial cells in the retina and optic nerve head. The significant decreases of NF and p–NF protein in the optic nerve appeared from 28 days after the injection. Reduction of cells in the RGCL was also observed 28 days after the injection, while, IPL thickness did not change.
ET–1 caused axonal degeneration and retinal neuronal cells death 28 days after the injection. The increase of p–ERK in the optic nerve and the retina may be involved in these processes.
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