Change in phospholipid species of retinal layer in traumatic optic neuropathy model
Change in phospholipid species of retinal layer in traumatic optic neuropathy model
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DOI：
10.1002/jnr.24500
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发表时间：
2019-08-05
影响因子：
4.2
通讯作者：
Yamada, Hisao
中科院分区：
文献类型：
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作者：
Hirahara, Yukie;Wakabayashi, Taketoshi;Yamada, Hisao
视神经损伤可导致几乎所有视网膜神经节细胞（RGC）死亡，并导致轴突缺失。到目前为止，我们已经研究了受伤的RGC轴突再生使用创伤性视神经损伤（TONI）啮齿动物模型，我们发现，轴突再生诱导自体外周神经移植。因此，轴突再生的有效途径需要RGC的环境调节。然而，TONI诱导的RGC环境仍然未知。在这里，我们详细分析了TONI后雌性和雄性C57 BL/6小鼠视网膜组织的变化，并集中在整个视网膜中富集的主要磷脂物质上。在损伤的视神经区域观察到反应性星形胶质细胞积聚、胶质瘢痕形成和脱髓鞘，而在视网膜层中检测到RGC细胞死亡、星形胶质细胞积聚和胶质细胞酸性蛋白（GFAP）阳性Muller细胞增加。此外，磷脂酰肌醇（PI）18：0/20：4定位于三个核层结构：神经节细胞层（GCL），内核层（INL），外核层（ONL）在对照组视网膜，但18：0/20：4 PI在TONI的定位被打乱。磷脂酰丝氨酸（PS）18：0/22：6染色结果显示，两种情况下均为内丛状层（IPL）特异性表达，且信号强度相似。其他PS物质和磷脂酰乙醇胺（PE）在视网膜层中的定位不同;然而，包括二十二碳六烯酸（DHA）在内的PE的表达受到TONI的影响。这些结果表明，不仅GCL，而且其他视网膜层的TONI的影响。
Injured optic nerves induce death in almost all retinal ganglion cells (RGC) and cause a loss of axons. To date, we have studied injured RGC axon regeneration by using a traumatic optic nerve injury (TONI) rodent model, and we revealed that axonal regeneration is induced by the graft of an autologous peripheral nerve. The efficient approach to the regeneration of axons thus needs an environmental adjustment of RGC. However, the RGC environment induced by TONI remains unknown. Here, we analyzed female and male C57BL/6 mouse retinal tissue alterations in detail after TONI and focused on the major phospholipid species that are enriched in the whole retina. Reactive astrocyte accumulation, glia scar formation, and demyelination were observed in the injured optic nerve area, while RGC cell death, astrocyte accumulation, and Glial fibrillary acidic protein (GFAP) positive Muller cell increases were detected in the retinal layer. Furthermore, phosphatidylinositol (PI) 18:0/20:4 was localized to three nuclear layer structures: the ganglion cell layer (GCL), the inner nuclear layer (INL), and the outer nuclear layer (ONL) in control retina; however, the localization of 18:0/20:4 PI in TONI was disturbed. Meanwhile, phosphatidylserine (PS) 18:0/22:6 showed that the expression was specifically in the inner plexiform layer (IPL) with similar signal intensity in both cases. Other PS species and phosphatidylethanolamine (PE) were differentially localized in the retinal layer; however, the expressions of PE including docosahexaenoic acid (DHA) were affected by TONI. These results suggest that not only GCL but also other retinal layers were influenced by TONI.