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首页> 外文期刊>The European Journal of Neuroscience >Lens injury stimulates adult mouse retinal ganglion cell axon regeneration via both macrophage- and lens-derived factors.
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Lens injury stimulates adult mouse retinal ganglion cell axon regeneration via both macrophage- and lens-derived factors.

机译：晶状体损伤通过巨噬细胞和晶状体来源的因子刺激成年小鼠视网膜神经节细胞轴突再生。

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Abstract In the present study the effects of lens injury on retinal ganglion cell axoneurite re-growth were investigated in adult mice. In vivo, lens injury promoted successful regeneration of retinal ganglion cell axons past the optic nerve lesion site, concomitant with the invasion of macrophages into the eye and the presence of activated retinal astrocytes/Muller cells. In vitro, retinal ganglion cells from lens-lesioned mice grew significantly longer neurites than those from intact mice, which correlated with the presence of enhanced numbers of activated retinal astrocytes/Muller cells. Co-culture of retinal ganglion cells from intact mice with macrophage-rich lesioned lens/vitreous body led to increased neurite lengths compared with co-culture with macrophage-free intact lens/vitreous body, pointing to a neurotrophic effect of macrophages. Furthermore, retinal ganglion cells from mice that had no lens injury but had received intravitreal Zymosan injections to stimulate macrophage invasion into the eye grew significantly longer neurites compared with controls, as did retinal ganglion cells from intact mice co-cultured with macrophage-rich vitreous body from Zymosan-treated mice. The intact lens, but not the intact vitreous body, exerted a neurotrophic effect on retinal ganglion cell neurite outgrowth, suggesting that lens-derived neurotrophic factor(s) conspire with those derived from macrophages in lens injury-stimulated axon regeneration. Together, these results show that lens injury promotes retinal ganglion cell axon regenerationeurite outgrowth in adult mice, an observation with important implications for axon regeneration studies in transgenic mouse models.
机译：摘要在本研究中，研究了晶状体损伤对成年小鼠视网膜神经节细胞轴突/神经突再生长的影响。在体内，晶状体损伤促进了视网膜神经节细胞轴突通过视神经病变部位的成功再生，并伴随着巨噬细胞侵入眼内以及激活的视网膜星形胶质细胞/穆勒细胞的存在。在体外，晶状体受损小鼠的视网膜神经节细胞比完整小鼠的神经节长得多，这与活化的视网膜星形胶质细胞/穆勒细胞数量的增加有关。与无巨噬细胞完整晶状体/玻璃体共培养相比，完整小鼠的视网膜神经节细胞与富含巨噬细胞的晶状体/玻璃体共培养导致神经突长度增加，这表明巨噬细胞具有神经营养作用。此外，与对照组相比，来自完整小鼠的视网膜神经节细胞与未培养的晶状体无损伤，但接受了玻璃体内酵母聚糖注射以刺激巨噬细胞侵入眼内，其视网膜神经节的生长明显比对照组长得多。来自酵母聚糖处理的小鼠。完整的晶状体，而不是完整的玻璃体，对视网膜神经节细胞神经突增生产生神经营养作用，表明晶状体来源的神经营养因子与巨噬细胞衍生的晶状体损伤刺激轴突再生合在一起。总之，这些结果表明，晶状体损伤促进了成年小鼠的视网膜神经节细胞轴突再生/神经突生长，这一发现对转基因小鼠模型中的轴突再生研究具有重要意义。

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