Soluble Nogo-66 receptor prevents synaptic dysfunction and rescues retinal ganglion cell loss in chronic glaucoma.

@article{Fu2011SolubleNR,
  title={Soluble Nogo-66 receptor prevents synaptic dysfunction and rescues retinal ganglion cell loss in chronic glaucoma.},
  author={Qing-ling Fu and Xin-Xue Liao and Xin Li and Dong Chen and Jianbo Shi and Weiping Wen and Daniel H. S. Lee and Kwok-fai So},
  journal={Investigative ophthalmology \& visual science},
  year={2011},
  volume={52 11},
  pages={
          8374-80
        }
}
  • Q. Fu, Xin-Xue Liao, K. So
  • Published 1 October 2011
  • Biology, Medicine
  • Investigative ophthalmology & visual science
PURPOSE Myelin inhibitory proteins inhibit axon growth and synaptic function by binding to the Nogo-66 receptor (NgR)1 in the central nervous system. Glaucoma is a progressive neuropathy characterized by loss of vision as a result of retinal ganglion cell (RGC) death. Synaptic degeneration is thought to be an early pathology of neurodegeneration in glaucoma and precedes RGC loss. The authors aimed to examine whether the NgR1 antagonist promotes synaptic recovery and RGC survival in glaucoma… 
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Neuroprotection of Retinal Ganglion Cells in Glaucoma by Blocking LINGO-1 Function or Using a Nogo-66 Receptor Antagonist
Nogo receptor 1 is expressed by nearly all retinal ganglion cells
TLDR
This work determines 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 NgR2 or Green Fluorescent Protein expressed under control of the ngr1 promoter, and demonstrates that more than 99% of RGCs express NgR 1.
Intravitreal delivery of human NgR-Fc decoy protein regenerates axons after optic nerve crush and protects ganglion cells in glaucoma models.
TLDR
Human NgR1(310)-Fc has favorable pharmacokinetics in the vitreal space and rescues large diameter RGC counts from increased IOP, and may have efficacy as a disease-modifying therapy for glaucoma.
Neuroprotective Strategies for Retinal Ganglion Cell Degeneration: Current Status and Challenges Ahead
TLDR
There is no therapeutic strategy directed to promote axonal regeneration of RGCs as a therapeutic approach for optic neuropathies, and the manipulation of several intrinsic and extrinsic factors has been proposed in order to stimulate axonal regenerate and functional repairing of axonal connections in the visual pathway.
Neuroprotective effects of antibodies on retinal ganglion cells in an adolescent retina organ culture
TLDR
It is detected that the tested antibodies have a protective effect on rgc which seems to be the result of reduced stress levels in the retina as well as a shift of glutamine synthetase localization in the endfeet of the Müller cells towards the inner retinal layer.
Hydrogen sulfide supplement attenuates the apoptosis of retinal ganglion cells in experimental glaucoma
Regulatory effects of inhibiting the activation of glial cells on retinal synaptic plasticity
TLDR
The results suggested that retinal glial cell activation might play an important role in the process of retinal synaptic plasticity induced by acute high intraocular pressure through affecting the expression and distribution of synaptic functional proteins, such as synaptophysin.
Neuronal Nogo-A upregulation does not contribute to ER stress-associated apoptosis but participates in the regenerative response in the axotomized adult retina
TLDR
A positive, cell-autonomous role is demonstrated for neuronal Nogo-A in the modulation of axonal regeneration in retinal ganglion cells after optic nerve injury in adult mice.
Limiting Neuronal Nogo Receptor 1 Signaling during Experimental Autoimmune Encephalomyelitis Preserves Axonal Transport and Abrogates Inflammatory Demyelination
TLDR
The data suggest that NgR1 governs axonal degeneration in the context of inflammatory-mediated demyelination through the phosphorylation of CRMP2 by stalling axonal vesicular transport, which could lead to therapeutic strategies to limit axonal damage and progressive MS.
Distribution of thrombospondins and their neuronal receptor α2δ1 in the rat retina.
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