Abstract
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.
Highlights
Damage to the retinal ganglion cell (RGC) axons that comprise the optic nerve (ON) can lead to loss of vision
In mice harboring one recombined allele and one wild-type (WT) allele (+) with the genotype, ngr1 Δ/+, nogo-66 receptor 1 (NgR1) is expressed from the WT allele (+), and green fluorescent protein (GFP) is expressed from the recombined conditional allele (Δ)under control of the ngr1 promoter
We first established that these mice express GFP in NgR1 immunoreactive cells in the ganglion cell layer (GCL), and showed that these cells included both RGCs and displaced amacrine cells
Summary
Damage to the retinal ganglion cell (RGC) axons that comprise the optic nerve (ON) can lead to loss of vision. These axons are affected in several diseases, including ON trauma, compression, ischemia, and glaucoma. A variety of intracellular and extracellular factors have been found to affect RGC survival and/or increase axon regeneration These include genes that alter intrinsic growth state such as Kruppel-like factor (Klf) transcription factors [1,2], the modulators of intraocular inflammation oncomodulin and dectin-1 [3,4,5,6], trophic factors including BDNF [7], the cell-intrinsic suppressors of regeneration pten [8,9], and cell-extrinsic inhibitors of regeneration that signal through the nogo-66 receptor 1 (NgR1) [10,11].
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