Absence of galectin-3 promotes neuroprotection in retinal ganglion cells after optic nerve injury
Absence of galectin-3 promotes neuroprotection in retinal ganglion cells after optic nerve injury
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DOI：
10.14670/hh-11-788
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发表时间：
2017-03-01
影响因子：
2
通讯作者：
Blanco Martinez, Ana Maria
中科院分区：
文献类型：
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作者：
Abreu, Carla Andreia;De Lima, Silmara Veline;Blanco Martinez, Ana Maria
成熟的中枢神经系统（CNS）的创伤通常会导致持续性缺陷，这是由于轴突在受伤后无法再生。越来越多的证据表明，促炎基因和促凋亡基因可能是促进视网膜神经节细胞神经保护的主要障碍，从而成功地促进轴突再生。本研究评估了半乳糖凝集素-3（Gal-3）缺乏对视神经挤压损伤后视网膜神经节细胞（RGC）存活和轴突再生/变性的影响。挤压后两周，与WT动物（495.4 +/- 53.96）相比，Gal-3-/-小鼠（1283 +/- 79.15）的细胞存活率增加了2.6倍。然而，在损伤后两周，在Gal-3-/-小鼠中没有观察到再生。此外，轴突变性在这些小鼠中呈现出特定的模式;电子显微镜（EM）分析显示不完全轴突变性，而WT小鼠呈现出晚期变性。这表明Gal 3-/-小鼠中神经纤维的去除可能是缺陷的，一旦神经中巨噬细胞/小胶质细胞的数量减少，这将导致沃勒变性过程的延迟。这项研究证明了Gal-3的缺乏如何影响损伤后RGC的存活和视神经再生/变性。我们的研究结果表明，Gal-3的缺失在RGC的存活中起着重要作用，因此可以成为RGC神经保护中治疗干预的潜在靶点。
A trauma to the mature central nervous system (CNS) often leads to persistent deficits, due to the inability of axons to regenerate after being injured. Increasing evidence suggests that pro-inflammatory and pro-apoptotic genes can present a major obstacle to promoting neuroprotection of retinal ganglion cells and consequently succeed in axonal regeneration. This study evaluated the effect of the absence of galectin-3 (Gal-3) on retinal ganglion cells (RGC) survival and axonal regeneration/degeneration after optic nerve crush injury. Two weeks after crush there was a 2.6 fold increase in the rate of cell survival in Gal-3-/- mice (1283 +/- 79.15) compared to WT animals (495.4 +/- 53.96). However, no regeneration was observed in the Gal-3-/- mice two weeks after lesion. Furthermore, axonal degeneration presented a particular pattern on those mice; Electron Microscopy (EM) analysis showed incomplete axon degeneration while the WT mice presented an advanced stage of degeneration. This suggests that the removal of the nerve fibers in the Gal 3-/- mice could be deficient and this would cause a delay in the process of Wallerian degeneration once there is a decrease in the number of macrophages/microglia in the nerve. This study demonstrates how the absence of Gal-3 can affect RGC survival and optic nerve regeneration/degeneration after lesion. Our results suggest that the absence of Gal-3 plays an important role in the survival of RGC and thus can be a potential target for therapeutic intervention in RGC neuroprotection.