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H. Takeda, Y. Kitaoka, H. Fujino, Y. Hayashi, Y. Munemasa, S. Ueno; Early Elevation of OX2 Antigen and OX2 Receptor in TNF--Induced Optic Nerve Neurodegeneration. Invest. Ophthalmol. Vis. Sci. 2008;49(13):3692.
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To evaluate the distribution of OX2 and its receptor within the optic nerve and to investigate the involvement of OX2/OX2R in TNF-α-induced optic nerve degeneration.
Eight weeks old male Wistar rats were treated with intravitreous injection of 10 ng TNF-α into one eye. PBS was administered as a control. Eyes were removed at 24 hr, 1 or 2 weeks after the injection. The protein levels of OX2 and OX2R in the optic nerve were examined by Western blot analysis. Expression of OX2 and OX2R were detected by immunohistochemistry.
Compared to control eyes, the protein levels of OX2 and OX2R were significantly increased 24 hr after TNF-α injection. Immunohistochemistry showed substantial increase in GFAP immunoreactivity in TNF-α treated eyes. Furthermore, our double-labeling immunohistochemical study showed that OX2 was co-localized with GFAP, but not neurofilament 24 hr after TNF-α injection.
We found that OX2 and its receptor were expressed in astrocytes, suggesting that OX2-OX2R pathway may play an important role as a glial response in TNF-α-induced optic nerve degeneration.
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