Brandli Alice, Gerhart Jacquelyn, Sutera Christopher K, Purushothuman Sivaraman, George-Weinstein Mindy, Stone Jonathan, Bravo-Nuevo Arturo
Bosch Institute and Discipline of Physiology, University of Sydney, Sydney, Australia.
Philadelphia College of Osteopathic Medicine, Philadelphia, PA, United States of America.
PLoS One. 2017 Jan 18;12(1):e0169744. doi: 10.1371/journal.pone.0169744. eCollection 2017.
To identify Myo/Nog cells in the adult retina and test their role in protecting retinal photoreceptors from light damage.
Light damage was induced by exposing albino rats raised in dim cyclic light to 1000 lux light for 24 hours. In one group of rats, Myo/Nog cells were purified from rat brain tissue by magnetic cell sorting following binding of the G8 monoclonal antibody (mAb). These cells were injected into the vitreous humour of the eye within 2 hours following bright light exposure. Retinal function was assessed using full-field, flash electroretinogram (ERG) before and after treatment. The numbers of Myo/Nog cells, apoptotic photoreceptors, and the expression of glial fibrillary acidic protein (GFAP) in Muller cells were assessed by immunohistochemistry.
Myo/Nog cells were present in the undamaged retina in low numbers. Light induced damage increased their numbers, particularly in the choroid, ganglion cell layer and outer plexiform layer. Intravitreal injection of G8-positive (G8+) cells harvested from brain mitigated all the effects of light damage examined, i.e. loss of retinal function (ERG), death of photoreceptors and the stress-induced expression of GFAP in Muller cells. Some of the transplanted G8+ cells were integrated into the retina from the vitreous.
Myo/Nog cells are a subpopulation of cells that are present in the adult retina. They increase in number in response to light induced stress. Intravitreal injection of Myo/Nog cells was protective to the retina, in part, by reducing retinal stress as measured by the Muller cell response. These results suggest that Myo/Nog cells, or the factors they produce, are neuroprotective and may be therapeutic in neurodegenerative retinal diseases.
鉴定成年视网膜中的肌动蛋白/诺吉细胞（Myo/Nog细胞），并测试它们在保护视网膜光感受器免受光损伤方面的作用。
将饲养在昏暗循环光照下的白化大鼠暴露于1000勒克斯光照下24小时，以诱导光损伤。在一组大鼠中，在G8单克隆抗体（mAb）结合后，通过磁性细胞分选从大鼠脑组织中纯化Myo/Nog细胞。在强光暴露后2小时内，将这些细胞注入眼玻璃体内。使用全视野闪光视网膜电图（ERG）在治疗前后评估视网膜功能。通过免疫组织化学评估Myo/Nog细胞的数量、凋亡的光感受器以及穆勒细胞中胶质纤维酸性蛋白（GFAP）的表达。
在未受损的视网膜中存在少量的Myo/Nog细胞。光诱导损伤增加了它们的数量，特别是在脉络膜、神经节细胞层和外丛状层。玻璃体内注射从脑中收获的G8阳性（G8+）细胞减轻了所检测的光损伤的所有影响，即视网膜功能丧失（ERG）、光感受器死亡以及穆勒细胞中应激诱导的GFAP表达。一些移植的G8+细胞从玻璃体整合到视网膜中。
Myo/Nog细胞是成年视网膜中存在的细胞亚群。它们的数量在光诱导应激下增加。玻璃体内注射Myo/Nog细胞对视网膜具有保护作用，部分原因是通过减少穆勒细胞反应所测量的视网膜应激。这些结果表明，Myo/Nog细胞或它们产生的因子具有神经保护作用，可能对神经退行性视网膜疾病具有治疗作用。
