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Protection of Pattern Electroretinogram and Retinal Ganglion Cells by Oncostatin M after Optic Nerve Injury

机译：视神经素对视神经损伤后的视网膜电图和视网膜神经节细胞的保护作用

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摘要

Injury to retinal ganglion cell (RGC) axons leads to selective loss of RGCs and vision. Previous studies have shown that exogenous neurotrophic factors promote RGC survival. We investigated the neuroprotective effects of oncostatin M (OSM), a member of the IL-6 family of cytokines, on pattern electroretinogram (PERG) and RGC survival after optic nerve crush (ON-crush) in the mouse. BALB/C mice received ON-crush in the left eyes for either 4-second or 1-second duration (4-s or 1-s). Fluoro-gold retrograde labeling was used to identify RGCs. RGC function was assessed by PERG measurement. OSM or CNTF protein was injected intravitreally immediately after ON-crush. OSM responsive cells were identified by localization of increased STAT3 phosphorylation. Significant higher RGC survival (46% of untreated control) was seen in OSM-treated eyes when assessed 2 weeks after 4-s ON-crush as compared to that (14% of untreated control) of the PBS-treated eyes (P<0.001). In addition, PERG amplitude was significantly higher in eyes treated with OSM or CNTF 1 week after 1-s ON-crush (36% of baseline) as compared with the amplitude of PBS-treated eyes (19% of the baseline, P = 0.003). An increase in STAT3 phosphorylation was localized in Müller layer after OSM treatment, suggesting that Müller cells mediate the effect of OSM. Our results demonstrate that one single injection of either OSM or CNTF after ON-crush improves RGC survival together with their electrophysiological activity. These data provide proof-of-concept for using neurotrophic factors OSM and CNTF for RGC degenerative diseases, including glaucoma and acute optic nerve trauma.
机译：视网膜神经节细胞（RGC）轴突的损伤导致RGC和视力的选择性丧失。先前的研究表明，外源性神经营养因子可促进RGC的存活。我们调查了抑癌素M（OSM）（一种IL-6家族细胞因子的成员）对小鼠视神经压迫（ON-Crush）后模式视网膜电图（PERG）和RGC存活的神经保护作用。 BALB / C小鼠在4秒或1秒的持续时间内（4 s或1 s）在左眼接受ON按压。荧光金逆行标记用于鉴定RGC。通过PERG测量评估RGC功能。 OS或CNTF蛋白在ON压后立即玻璃体内注射。 OSM反应性细胞是通过增加STAT3磷酸化定位来鉴定的。当在4秒钟ON击打后2周评估，在OSM治疗的眼睛中观察到的RGC存活率显着更高（未治疗的对照组的46％），而在PBS治疗的眼睛中，RGC的存活率（未治疗的对照组的14％）更高（P <0.001 ）。此外，在经过1秒钟ON按压后1周，接受OSM或CNTF治疗的眼睛的PERG幅度（基线的36％）明显高于接受PBS处理的眼睛的幅度（基线的19％，P = 30.003） ）。 OSM处理后，STAT3磷酸化的增加位于Müller层，这表明Müller细胞介导OSM的作用。我们的结果表明，ON粉碎后单次注射OSM或CNTF可以改善RGC存活率及其电生理活性。这些数据提供了将神经营养因子OSM和CNTF用于RGC退行性疾病（包括青光眼和急性视神经损伤）的概念验证。

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