Lens injury stimulates axon regeneration in the mature rat optic nerve
Lens injury stimulates axon regeneration in the mature rat optic nerve
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DOI：
10.1523/jneurosci.20-12-04615.2000
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发表时间：
2000-06-15
影响因子：
5.3
通讯作者：
Benowitz, LI
中科院分区：
文献类型：
--
作者：
Leon, S;Yin, YQ;Benowitz, LI
在成熟哺乳动物中，视网膜神经节细胞(RGC)在视神经损伤后不能再生轴突，很快就会发生细胞凋亡。然而，晶状体上的一个小伤口可以提高RGC的存活率，并使这些细胞能够将其轴突再生到视神经正常抑制的环境中。即使在视神经完好的情况下，晶状体损伤也会刺激巨噬细胞渗入眼睛，激活Muller细胞，并增加整个视网膜神经节细胞中GAP-43的表达。相比之下，单独或联合眼内注射不损害晶状体的轴突切断术，只会导致RGC中GAP-43表达的微小变化，并对其他类型的细胞产生最小的激活。将神经损伤与晶状体穿刺术相结合，可使RGC存活率增加8倍，并使在挤压部位以外再生的轴突数量增加100倍。巨噬细胞的激活似乎发挥了关键作用，因为眼内注射酵母细胞壁制剂酵母多糖，在没有晶状体损伤的情况下刺激单核细胞，并诱导RGC再生它们的轴突进入远端视神经。
In mature mammals, retinal ganglion cells (RGCs) are unable to regenerate their axons after optic nerve injury, and they soon undergo apoptotic cell death. However, a small puncture wound to the lens enhances RGC survival and enables these cells to regenerate their axons into the normally inhibitory environment of the optic nerve. Even when the optic nerve is intact, lens injury stimulates macrophage infiltration into the eye, Muller cell activation, and increased GAP-43 expression in ganglion cells across the entire retina. In contrast, axotomy, either alone or combined with intraocular injections that do not infringe on the lens, causes only a minimal change in GAP-43 expression in RGCs and a minimal activation of the other cell types. Combining nerve injury with lens puncture leads to an eightfold increase in RGC survival and a 100-fold increase in the number of axons regenerating beyond the crush site. Macrophage activation appears to play a key role, because intraocular injections of Zymosan, a yeast cell wall preparation, stimulated monocytes in the absence of lens injury and induced RGCs to regenerate their axons into the distal optic nerve.