PROGRAMMED CELL-DEATH OF RETINAL GANGLION-CELLS DURING EXPERIMENTAL GLAUCOMA
PROGRAMMED CELL-DEATH OF RETINAL GANGLION-CELLS DURING EXPERIMENTAL GLAUCOMA
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DOI：
10.1016/s0014-4835(95)80056-5
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发表时间：
1995-07-01
影响因子：
3.4
通讯作者：
SHARMA, SC
中科院分区：
文献类型：
--
作者：
GARCIAVALENZUELA, E;SHAREEF, S;SHARMA, SC
青光眼期间视网膜神经节细胞的死亡被认为是由于轴突通过筛板离开眼睛时受到损伤所致。在这项研究中，通过烧灼两条角膜缘来源的静脉，将大鼠的眼压升高至正常平均值的两倍。为了研究青光眼眼中的视网膜神经节细胞是否遵循细胞凋亡类型的死亡，使用一种通过外源末端脱氧核苷酸转移酶将生物素化脱氧核苷酸特异性掺入 DNA 3'-OH 末端的方法对细胞核中的 DNA 断裂进行原位标记。给予蛋白质合成抑制剂放线菌酮后，生物素标记的细胞核数量减少证明了死亡机制的活性。我们的结果表明，当眼压显着升高时，成年大鼠的视网膜神经节细胞通过凋亡而死亡。通过神经元死亡程序的潜在可中断性，这为治疗视网膜青光眼损伤带来了新的可能性。 (C) 1995 学术出版社有限公司
The death of retinal ganglion cells during glaucoma is thought to result from damage to their axons as they exit the eye through the lamina cribrosa. In this study, intraocular pressure in the rat was increased to twice the normal averge by cauterizing two limbal-derived veins. To investigate whether retinal ganglion cells in the glaucomatous eye follow an apoptotic type of death, DNA breaks in nuclei were labeled in situ, using a method that specifically incorporates biotinylated deoxynucleotides by exogenous terminal deoxynucleotidyl transferase to the 3'-OH ends of DNA. The active nature of the death mechanism was demonstrated by the reduction in numbers of biotin-labeled nuclei after administration of the protein synthesis inhibitor, cycloheximide. Our results suggest that retinal ganglion cells of the adult rat die through apoptosis when the intraocular pressure is markedly increased. This raises new possibilities in the treatment of glaucomatous damage to the retina, by the potential interruptibility of a program for neuronal death. (C) 1995 Academic Press Limited