期刊
EXPERIMENTAL NEUROLOGY
卷 209, 期 2, 页码 469-482出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.expneurol.2007.09.020
关键词
retina; optic nerve; axon regeneration; retinal ganglion cells; macrophages; oncomodulin; zymosan; CNS
Retinal ganglion cells (RGCs) cannot regenerate their axons after injury and undergo apoptosis soon after an intraorbital injury of the optic nerve. However, RGCs reactivate their axonal growth program when inflammatory reactions occur in the eye, which enables them to survive axotomy and to regenerate lengthy axons into the lesioned optic nerve. Lens injury (LI) and zymosan injections can induce these beneficial processes and provoke also a strong accumulation of activated macrophages in the vitreous body. It has recently been suggested that macrophage-derived oncomodulin is the principal mediator of this phenomenon. We show here that oncomodulin is not significantly expressed in primary macrophages and that the intraocular levels of this protein do not increase after LI or zymosan treatment. Furthermore, greatly reducing the invasion of macrophages into the inner eye does not diminish the neuroprotective effects of LI, but rather increases axon regeneration into the optic nerve. Axon regeneration is correlated with the activation of retinal astrocytes and Muller cells. Our data suggest that intraocular inflammation mediates its main beneficial effects through factors other than oncomodulin and that the underlying mechanism might be independent of the presence of activated macrophages. (C) 2007 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据