[Effect of Nogo-66 on retinal microglia in chronic ocular hypertension rats].

ABSTRACT

OBJECTIVE: To study the effect of protein Nogo-66 on the expression of CD11b and MHC-II in retinal microglia of chronic ocular hypertension SD rats and the effects of protein Nogo-66 on the immunogenicity of injured retinal tissues. METHODS: It was a control experimental study. Chronic ocular hypertension rat model was established by laser photocoagulation on the anterior chamber angle and superficial vein of the sclera. One ml of Nogo-66 (0.01%) in PBS was injected subcutaneously on the day of laser treatment and 0.005% Nogo-66 PBS solution was injected into the vitreous 7 days and 1 month latter. PBS without Nogo-66 was injected in the control group. The expression of cell surface antigen CD11b and MHC-II were detected by immunohistochemistry 1 month and 1 day after the establishment of hypertension model. The difference of average IOP among groups was analyzed by variance analysis. The difference of expression of CD11b and MHC-II between the experimental and control groups was analyzed by t-test. RESULTS: The intraocular pressure (IOP) of experimental groups rised from the seventh day after model-building and the highest IOP was (24.16 ± 2.70) mm Hg (1 mm Hg = 0.133 kPa) 1 month later while that in the control groups was (15.93 ± 3.28) mm Hg. The difference between them was statistically significant (F = 2.10, P < 0.05). Expression of CD11b was (1.78 ± 0.63)% and MHC-II was (3.92 ± 1.03)% in Nogo-66 with hypertension groups, these results was significantly lower than those in Nogo-66 with normal intraocular pressure groups in which the expression of CD11b was (8.15 ± 1.97)% (t = 2.35, P < 0.05) and MHC-II was (11.45 ± 1.97)% (t = 2.14, P < 0.05). CONCLUSIONS: Protein Nogo-66 activated the cell surface antigen CD11b in nerve fiber layer of retina and induced antigen presenting molecules (MHC-II). This indicates that Nogo has the center immunogenicity and this protein could activate antigen-presenting cells to present injury antigen.