Nogo receptor 1 is expressed by nearly all retinal ganglion cells

• 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
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0196565

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.