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Soluble Nogo-66 receptor prevents synaptic dysfunction and rescues retinal ganglion cell loss in chronic glaucoma.
Invest Ophthalmol Vis Sci. 2011 Oct 28; 52(11):8374-80.IO

Abstract

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.

METHODS

Experimental ocular hypertension model was induced in adult rats with laser coagulation of the episcleral and limbal veins. NgR1 antagonist, soluble NgR1 (sNgR-Fc) was administrated to examine their effect on synaptic recovery and RGC survival. Expression of c-Fos, a neuronal connectivity marker, in the retinas was investigated using immunohistochemistry.

RESULTS

NgR1 was expressed in RGCs and upregulated after intraocular pressure elevation. Treatment with sNgR-Fc significantly reduced RGC loss at 2 and 4 weeks after the induction of ocular hypertension and also promoted RGC survival after optic nerve transection. There was no RGC loss at 5 days but there was significant synaptic degeneration as measured by c-Fos. Administration of sNgR-Fc attenuated synaptic degeneration at 5 days, and at 2 and 4 weeks.

CONCLUSIONS

These data suggest that synaptic degeneration may be an initial molecular mechanism for neurodegeneration in glaucoma and appropriate NgR1 antagonism may delay the progression of the disease.

Authors+Show Affiliations

Otorhinolaryngology Hospital, Guangzhou,Guangdong, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21948553

Citation

Fu, Qing-Ling, et al. "Soluble Nogo-66 Receptor Prevents Synaptic Dysfunction and Rescues Retinal Ganglion Cell Loss in Chronic Glaucoma." Investigative Ophthalmology & Visual Science, vol. 52, no. 11, 2011, pp. 8374-80.
Fu QL, Liao XX, Li X, et al. Soluble Nogo-66 receptor prevents synaptic dysfunction and rescues retinal ganglion cell loss in chronic glaucoma. Invest Ophthalmol Vis Sci. 2011;52(11):8374-80.
Fu, Q. L., Liao, X. X., Li, X., Chen, D., Shi, J., Wen, W., Lee, D. H., & So, K. F. (2011). Soluble Nogo-66 receptor prevents synaptic dysfunction and rescues retinal ganglion cell loss in chronic glaucoma. Investigative Ophthalmology & Visual Science, 52(11), 8374-80. https://doi.org/10.1167/iovs.11-7667
Fu QL, et al. Soluble Nogo-66 Receptor Prevents Synaptic Dysfunction and Rescues Retinal Ganglion Cell Loss in Chronic Glaucoma. Invest Ophthalmol Vis Sci. 2011 Oct 28;52(11):8374-80. PubMed PMID: 21948553.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Soluble Nogo-66 receptor prevents synaptic dysfunction and rescues retinal ganglion cell loss in chronic glaucoma. AU - Fu,Qing-Ling, AU - Liao,Xin-Xue, AU - Li,Xin, AU - Chen,Dong, AU - Shi,Jianbo, AU - Wen,Weiping, AU - Lee,Daniel H S, AU - So,Kwok-Fai, Y1 - 2011/10/28/ PY - 2011/9/28/entrez PY - 2011/9/29/pubmed PY - 2012/1/5/medline SP - 8374 EP - 80 JF - Investigative ophthalmology & visual science JO - Invest Ophthalmol Vis Sci VL - 52 IS - 11 N2 - 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. METHODS: Experimental ocular hypertension model was induced in adult rats with laser coagulation of the episcleral and limbal veins. NgR1 antagonist, soluble NgR1 (sNgR-Fc) was administrated to examine their effect on synaptic recovery and RGC survival. Expression of c-Fos, a neuronal connectivity marker, in the retinas was investigated using immunohistochemistry. RESULTS: NgR1 was expressed in RGCs and upregulated after intraocular pressure elevation. Treatment with sNgR-Fc significantly reduced RGC loss at 2 and 4 weeks after the induction of ocular hypertension and also promoted RGC survival after optic nerve transection. There was no RGC loss at 5 days but there was significant synaptic degeneration as measured by c-Fos. Administration of sNgR-Fc attenuated synaptic degeneration at 5 days, and at 2 and 4 weeks. CONCLUSIONS: These data suggest that synaptic degeneration may be an initial molecular mechanism for neurodegeneration in glaucoma and appropriate NgR1 antagonism may delay the progression of the disease. SN - 1552-5783 UR - https://www.unboundmedicine.com/medline/citation/21948553/Soluble_Nogo_66_receptor_prevents_synaptic_dysfunction_and_rescues_retinal_ganglion_cell_loss_in_chronic_glaucoma_ L2 - https://iovs.arvojournals.org/article.aspx?doi=10.1167/iovs.11-7667 DB - PRIME DP - Unbound Medicine ER -