Nogo receptor 1 is expressed by nearly all retinal ganglion cells

A variety of conditions ranging from glaucoma to blunt force trauma lead to optic nerve atrophy. Identifying signaling pathways for stimulating axon growth in the optic nerve may lead to treatments for these pathologies. Inhibiting signaling by the nogo-66 receptor 1 (NgR1) promotes the re-extension...

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Published in:PloS one 2018-05, Vol.13 (5), p.e0196565-e0196565
Main Authors: Solomon, Alexander M, Westbrook, Teleza, Field, Greg D, McGee, Aaron W
Format: Article
Language:English
Subjects:
Analysis
Animals
Antibodies
Atrophy
Axons
Axons - metabolism
Biology and Life Sciences
Cell death
Fluorescence
Gene Expression
Genetic aspects
Glaucoma
Green fluorescent protein
Green Fluorescent Proteins - metabolism
Immunohistochemistry
Medicine
Medicine and Health Sciences
Mice
Mice, Knockout
Mice, Transgenic
Morphology
mRNA
Nerve Regeneration - genetics
Nerve Regeneration - physiology
Nervous system
Neurobiology
Neurons
Neurosciences
Nogo protein
Nogo Receptor 1 - deficiency
Nogo Receptor 1 - genetics
Nogo Receptor 1 - metabolism
Optic nerve
Optic Nerve - metabolism
Optic Nerve - physiology
Optic Nerve Injuries - genetics
Optic Nerve Injuries - metabolism
Optic Nerve Injuries - pathology
Pediatrics
Physiological aspects
Proteins
Regeneration
Research and Analysis Methods
Retina
Retinal cells
Retinal ganglion cells
Retinal Ganglion Cells - metabolism
Retinal Ganglion Cells - pathology
Risk factors
RNA, Messenger - genetics
RNA, Messenger - metabolism
Rodents
Signal Transduction
Signaling
Trauma
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cited_by cdi_FETCH-LOGICAL-c692t-fe37becafa374f7883f9074ee43b6a950fe8531492ca558c799d524e2b09ab083
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description A variety of conditions ranging from glaucoma to blunt force trauma lead to optic nerve atrophy. Identifying signaling pathways for stimulating axon growth in the optic nerve may lead to treatments for these pathologies. Inhibiting signaling by the nogo-66 receptor 1 (NgR1) promotes the re-extension of axons following a crush injury to the optic nerve, and while NgR1 mRNA and protein expression are observed in the retinal ganglion cell (RGC) layer and inner nuclear layer, which retinal cell types express NgR1 remains unknown. Here we determine the expression pattern of NgR1 in the mouse retina by co-labeling neurons with characterized markers of specific retinal neurons together with antibodies specific for NgR1 or Green Fluorescent Protein expressed under control of the ngr1 promoter. We demonstrate that more than 99% of RGCs express NgR1. Thus, inhibiting NgR1 function may ubiquitously promote the regeneration of axons by RGCs. These results provide additional support for the therapeutic potential of NgR1 signaling in reversing optic nerve atrophy.
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identifier ISSN: 1932-6203
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1932-6203
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source Publicly Available Content Database (Proquest) (PQ_SDU_P3); PubMed Central
subjects Analysis
Animals
Antibodies
Atrophy
Axons
Axons - metabolism
Biology and Life Sciences
Cell death
Fluorescence
Gene Expression
Genetic aspects
Glaucoma
Green fluorescent protein
Green Fluorescent Proteins - metabolism
Immunohistochemistry
Medicine
Medicine and Health Sciences
Mice
Mice, Knockout
Mice, Transgenic
Morphology
mRNA
Nerve Regeneration - genetics
Nerve Regeneration - physiology
Nervous system
Neurobiology
Neurons
Neurosciences
Nogo protein
Nogo Receptor 1 - deficiency
Nogo Receptor 1 - genetics
Nogo Receptor 1 - metabolism
Optic nerve
Optic Nerve - metabolism
Optic Nerve - physiology
Optic Nerve Injuries - genetics
Optic Nerve Injuries - metabolism
Optic Nerve Injuries - pathology
Pediatrics
Physiological aspects
Proteins
Regeneration
Research and Analysis Methods
Retina
Retinal cells
Retinal ganglion cells
Retinal Ganglion Cells - metabolism
Retinal Ganglion Cells - pathology
Risk factors
RNA, Messenger - genetics
RNA, Messenger - metabolism
Rodents
Signal Transduction
Signaling
Trauma
title Nogo receptor 1 is expressed by nearly all retinal ganglion cells
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