Autophagy in retinal ganglion cells in a rhesus monkey chronic hypertensive glaucoma model.
Autophagy in retinal ganglion cells in a rhesus monkey chronic hypertensive glaucoma model.
复制标题
恒河猴慢性高血压青光眼模型视网膜神经节细胞的自噬
DOI：
10.1371/journal.pone.0077100
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Zhuo Y
中科院分区：
文献类型：
--
作者：
Deng S;Wang M;Yan Z;Tian Z;Chen H;Yang X;Zhuo Y
Primary open angle glaucoma (POAG) is a neurodegenerative disease characterized by physiological intraocular hypertension that causes damage to the retinal ganglion cells (RGCs). In the past, RGC damage in POAG was suggested to have been attributed to RGC apoptosis. However, in the present study, we applied a model closer to human POAG through the use of a chronic hypertensive glaucoma model in rhesus monkeys to investigate whether another mode of progressive cell death, autophagy, was activated in the glaucomatous retinas. First, in the glaucomatous retinas, the levels of LC3B-II, LC3B-II/LC3B-I and Beclin 1 increased as demonstrated by Western blot analyses, whereas early or initial autophagic vacuoles (AVi) and late or degraded autophagic vacuoles (AVd) accumulated in the ganglion cell layer (GCL) and in the inner plexiform layer (IPL) as determined by transmission electron microscopy (TEM) analysis. Second, lysosome activity and autophagosome-lysosomal fusion increased in the RGCs of the glaucomatous retinas, as demonstrated by Western blotting against lysosome associated membrane protein-1 (LAMP1) and double labeling against LC3B and LAMP1. Third, apoptosis was activated in the glaucomatous eyes with increased levels of caspase-3 and cleaved caspase-3 and an increased number of TUNEL-positive RGCs. Our results suggested that autophagy was activated in RGCs in the chronic hypertensive glaucoma model of rhesus monkeys and that autophagy may have potential as a new target for intervention in glaucoma treatment.
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影响因子：
7.8
作者：
Demarchi, Francesca;Bertoli, Cosetta;Copetti, Tamara;Tanida, Isei;Brancolini, Claudio;Eskelinen, Eeva-Liisa;Schneider, Claudio
通讯作者：
Schneider, Claudio
影响因子：
9
作者：
通讯作者：
--
影响因子：
4.1
作者：
Foster, PJ;Buhrmann, R;Johnson, GJ
通讯作者：
Johnson, GJ
影响因子：
3.7
作者：
Piras A;Gianetto D;Conte D;Bosone A;Vercelli A
通讯作者：
Vercelli A
DOI：
10.1083/jcb.200412022
发表时间：
2005-05-09
期刊：
The Journal of cell biology
影响因子：
--
作者：
Komatsu M;Waguri S;Ueno T;Iwata J;Murata S;Tanida I;Ezaki J;Mizushima N;Ohsumi Y;Uchiyama Y;Kominami E;Tanaka K;Chiba T
通讯作者：
Chiba T