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R. Sanchez, Y. Kitaoka, A.A. Sadun, T.T. Lam; IL–6R and gp130 in Retinal Ischemia Reperfusion Injury in Rats . Invest. Ophthalmol. Vis. Sci. 2005;46(13):5318.
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Purpose: Previously, we published a report implicating that endogenous IL–6 and IL–6 Receptor (IL–6R) in the retinal ganglion cells (RGCs) may play a role in RGC survival after an ischemia–reperfusion insult. This study further examines the role of IL–6R and its associated complex gp130. Methods: A published method of inducing ischemia–reperfusion injury by raising the intraocular pressure with a saline column was used. After 60–minutes of non–perfusion, the retinas were allowed to reperfuse. Vehicle, anti–IL–6R antibody (2.5 µg), anti–gp130 antibody (2.5 µg), or a combination of the two antibodies (each at 2.5 µg) were immediately injected into the vitreous bodies of groups of animals. Seven days after I/R injury, the animals were euthanized and the effect on Retinal Ganglion Cell Layer Cell (RGCLC) loss was evaluated using a previously described procedure for flat mounted whole retinas, cresyl violet staining and cell counting. Results: Injection of either IL–6R or gp130 antibody appeared to aggravate the loss of RGCLCs after I/R injury and their combination gave statistically significant lowered numbers of RGCLCs in the central (1341.484 ± 133.478 RGCLCs/mm2; P<0.001 vs. vehicle, Dunnett's Method) and peripheral (1318.980 ± 125.946 RGCLCs/mm2; P<0.001 vs. vehicle, Dunnett's Method) retinas than the corresponding vehicle treated retinas. Conclusions: Endogenous IL–6R and its gp130 may be important for RGCLC survival after I/R injury.
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