实验性青光眼视网膜胶质细胞的活化与神经节细胞的变性有关

IF 18.6 1区 医学 Q1 OPHTHALMOLOGY
Yanying Miao , Guo-Li Zhao , Shuo Cheng, Zhongfeng Wang, Xiong-Li Yang
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引用次数: 10

摘要

眼压升高是青光眼神经退行性变的主要危险因素。神经胶质细胞在视网膜神经元的正常功能中起重要作用,在IOP升高引起的实验性青光眼动物模型中参与视网膜神经节细胞(RGC)变性。在IOP升高的情况下,mGluR I首先被激活,Kir4.1通道随后被抑制,这导致了 ller细胞的激活。 ller细胞活化后是一个复杂的过程,包括增殖、炎症和生长因子的释放(胶质瘤)。胶质瘤进一步受到几个因素的调控。活化的m ller细胞通过产生谷氨酸受体介导的兴奋性毒性,释放细胞毒性因子和诱导小胶质细胞活化来促进RGC变性。IOP升高激活了小胶质细胞,在形态和功能发生变化后,这些细胞作为视网膜中的常驻免疫细胞,表现出适应性免疫反应,包括促炎因子(肿瘤神经官能因子-α、白细胞介素等)的释放增强。这些ATP和toll样受体介导的反应受到热休克蛋白、CD200R、趋化因子受体和代谢嘌呤能受体的进一步调节,可能会加重RGC损失。在视神经头,星形胶质细胞形成是一个复杂的反应过程,包括嘌呤、递质、趋化因子、生长因子和细胞因子,通过释放促炎因子和改变细胞外基质导致青光眼RGC轴突损伤。活化的神经胶质细胞对RGCs的作用通过不同类型的神经胶质细胞之间的相互作用而进一步改变。最后,对该领域未来可能的研究方向进行了深入的讨论。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Activation of retinal glial cells contributes to the degeneration of ganglion cells in experimental glaucoma

Elevation of intraocular pressure (IOP) is a major risk factor for neurodegeneration in glaucoma. Glial cells, which play an important role in normal functioning of retinal neurons, are well involved into retinal ganglion cell (RGC) degeneration in experimental glaucoma animal models generated by elevated IOP. In response to elevated IOP, mGluR I is first activated and Kir4.1 channels are subsequently inhibited, which leads to the activation of Müller cells. Müller cell activation is followed by a complex process, including proliferation, release of inflammatory and growth factors (gliosis). Gliosis is further regulated by several factors. Activated Müller cells contribute to RGC degeneration through generating glutamate receptor-mediated excitotoxicity, releasing cytotoxic factors and inducing microglia activation. Elevated IOP activates microglia, and following morphological and functional changes, these cells, as resident immune cells in the retina, show adaptive immune responses, including an enhanced release of pro-inflammatory factors (tumor neurosis factor-α, interleukins, etc.). These ATP and Toll-like receptor-mediated responses are further regulated by heat shock proteins, CD200R, chemokine receptors, and metabotropic purinergic receptors, may aggravate RGC loss. In the optic nerve head, astrogliosis is initiated and regulated by a complex reaction process, including purines, transmitters, chemokines, growth factors and cytokines, which contributes to RGC axon injury through releasing pro-inflammatory factors and changing extracellular matrix in glaucoma. The effects of activated glial cells on RGCs are further modified by the interplay among different types of glial cells. This review is concluded by presenting an in-depth discussion of possible research directions in this field in the future.

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来源期刊
CiteScore
34.10
自引率
5.10%
发文量
78
期刊介绍: Progress in Retinal and Eye Research is a Reviews-only journal. By invitation, leading experts write on basic and clinical aspects of the eye in a style appealing to molecular biologists, neuroscientists and physiologists, as well as to vision researchers and ophthalmologists. The journal covers all aspects of eye research, including topics pertaining to the retina and pigment epithelial layer, cornea, tears, lacrimal glands, aqueous humour, iris, ciliary body, trabeculum, lens, vitreous humour and diseases such as dry-eye, inflammation, keratoconus, corneal dystrophy, glaucoma and cataract.
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