Jia-Wei Wang1, Shi-Da Chen, Xiu-Lan Zhang, Jost B Jonas. 1. *State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, P.R. China †Department of Ophthalmology, Medical Faculty Mannheim of the Ruprecht-Karls-University, Heidelberg, Germany.
Abstract
OBJECTIVE: To review the current research on microglia as it relates to glaucoma, and summarize the potential microglia-targeted therapies. DATA SOURCES: The data were collected from PubMed and Google Scholar databases published in English up to July 2014. Keywords used, both alone and in combination, in the database search included retinal microglia, over-activation and inhibition of microglia, and glaucoma. STUDY SELECTION: Articles were selected and reviewed if they involved microglia in animal models or human patients with glaucoma. Moreover, we also cited some comprehensive amalgamation of published literature. RESULTS: Together with the macroglia [astrocytes, ependymal cells, oligodendrocytes, radial (Müller) cells], the microglia form the supportive tissue of the central nervous system (CNS). Glial cells are generally smaller than the neural cells, but outnumber them by a factor of 5 to 10 with marked regional differences in the CNS. Approximately half of the volume of the CNS is composed of glial cells. Because of the blood-retina barrier, blood-born immunologic cells cannot penetrate into the retina under physiological conditions; the retinal microglial cells are the primary immunocompetent cells in the retina. The microglial cells are involved in any process of cell degeneration and loss, including retinal ganglion fiber and cell loss. Surveying the retinal tissue in normal situations as "spiders in a net," the retinal microglial cells change their form from a resting dendritic-like shape to an activated ameboid form in the case of invading microorganisms or cell damage. They are involved in the process of cell apoptosis and removal of the dead cells. Studies suggested that inhibition of the microglial cell activation in the case of optic nerve damage can increase the number of surviving retinal ganglion cells and may thus be neuroprotective. CONCLUSIONS: Activated microglia appear early in the glaucomatous process and may contribute detrimentally to the neuronal apoptosis in the later stage. Neuroprotective strategies that inhibit activated microglia may provide novel treatment modalities for glaucomatous optic neuropathy and any other retinal and optic nerve disease.
OBJECTIVE: To review the current research on microglia as it relates to glaucoma, and summarize the potential microglia-targeted therapies. DATA SOURCES: The data were collected from PubMed and Google Scholar databases published in English up to July 2014. Keywords used, both alone and in combination, in the database search included retinal microglia, over-activation and inhibition of microglia, and glaucoma. STUDY SELECTION: Articles were selected and reviewed if they involved microglia in animal models or humanpatients with glaucoma. Moreover, we also cited some comprehensive amalgamation of published literature. RESULTS: Together with the macroglia [astrocytes, ependymal cells, oligodendrocytes, radial (Müller) cells], the microglia form the supportive tissue of the central nervous system (CNS). Glial cells are generally smaller than the neural cells, but outnumber them by a factor of 5 to 10 with marked regional differences in the CNS. Approximately half of the volume of the CNS is composed of glial cells. Because of the blood-retina barrier, blood-born immunologic cells cannot penetrate into the retina under physiological conditions; the retinal microglial cells are the primary immunocompetent cells in the retina. The microglial cells are involved in any process of cell degeneration and loss, including retinal ganglion fiber and cell loss. Surveying the retinal tissue in normal situations as "spiders in a net," the retinal microglial cells change their form from a resting dendritic-like shape to an activated ameboid form in the case of invading microorganisms or cell damage. They are involved in the process of cell apoptosis and removal of the dead cells. Studies suggested that inhibition of the microglial cell activation in the case of optic nerve damage can increase the number of surviving retinal ganglion cells and may thus be neuroprotective. CONCLUSIONS: Activated microglia appear early in the glaucomatous process and may contribute detrimentally to the neuronal apoptosis in the later stage. Neuroprotective strategies that inhibit activated microglia may provide novel treatment modalities for glaucomatous optic neuropathy and any other retinal and optic nerve disease.
Authors: Maria H Madeira; Arturo Ortin-Martinez; Francisco Nadal-Nícolas; António F Ambrósio; Manuel Vidal-Sanz; Marta Agudo-Barriuso; Ana Raquel Santiago Journal: Sci Rep Date: 2016-06-08 Impact factor: 4.379