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Siponimod exerts neuroprotective effects on the retina and higher visual pathway through neuronal S1PR1 in experimental glaucoma

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Neural Regeneration Research 2023年第4期18卷 840-848页

作者： Devaraj Basavarajappa Vivek Gupta Nitin Chitranshi Roshana Vander Wall Rashi Rajput Kanishka Pushpitha Samridhi Sharma Mehdi Mirzaei alexander klistorner Stuart L.Graham Department of Clinical Medicine Faculty of MedicineHealth and Human SciencesMacquarie UniversityNorth RydeSydneyNSWAustralia

Sphingosine-1-phosphate receptor(S1PR)signaling regulates diverse pathophysiological processes in the central nervous system.The role of S1PR signaling in neurodegenerative conditions is still largely unidentified.Siponimod is a specific modulator of S1P1 and S1P5 receptors,an immunosuppressant drug for managing secondary progressive multiple sclerosis.We investigated its neuroprotective properties in vivo on the retina and the brain in an optic nerve injury model induced by a chronic increase in intraocular pressure or acute N-methyl-D-aspartate excitotoxicity.Neuronal-specific deletion of sphingosine-1-phosphate receptor(S1PR1)was carried out by expressing AAV-PHP.eB-Cre recombinase under Syn1 promoter in S1PR1mice to define the role of S1PR1 in neurons.Inner retinal electrophysiological responses,along with histological and immunofluorescence analysis of the retina and optic nerve tissues,indicated significant neuroprotective effects of siponimod when administered orally via diet in chronic and acute optic nerve injury models.Further,siponimod treatment showed significant protection against trans-neuronal degenerative changes in the higher visual center of the brain induced by optic nerve injury.Siponimod treatment also reduced microglial activation and reactive gliosis along the visual pathway.Our results showed that siponimod markedly upregulated neuroprotective Akt and Erk1/2 activation in the retina and the brain.Neuronal-specific deletion of S1PR1 enhanced retinal and dorsolateral geniculate nucleus degenerative changes in a chronic optic nerve injury condition and attenuated protective effects of siponimod.In summary,our data demonstrated that S1PR1signaling plays a vital role in the retinal ganglion cell and dorsolateral geniculate nucleus neuronal survival in experimental glaucoma,and siponimod exerts direct neuroprotective effects through S1PR1 in neurons in the central nervous system independent of its peripheral immuno-modulatory effects.Our findings suggest that neuronal S1PR1 is a neuroprotective

关键词： glaucoma intraocular pressure neurodegeneration neuroprotection optic nerve injury retinal ganglion cells siponimod sphingosine-1-phosphate

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Mechanism of delayed conduction of fellow eyes in patients with optic neuritis

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International Journal of Ophthalmology(English edition) 2018年第2期11卷 329-332页

作者： Daniah Alshowaeir Con Yiannikas Clare Fraser alexander klistorner Department of Ophthalmology University of Sydney Department of Ophthalmology King Saud University Department of Neurology Concord Hospital Department of Neurology Royal North Shore Hospital Australian School of Advanced Medicine Macquarie University

To test the hypothesis that latency delay in the fellow eyes of optic neuritis（ON） patients and to compensate for delayed transmission of visual information, latency change of multi-focal visual evoked potential（mf VEP） traces in fellow eyes of 15 ON patients were analyzed. Patients with low risk（LR） for developing multiple sclerosis（MS） were examined separately from MS patients to isolate effect of cortical plasticity from potential pathological changes in disseminated disease. The small increase in latency in fellow eyes of LR group was statistically not significant. In MS patients, the latency was significantly delayed（P〈0.02）. The magnitude of the latency change in the fellow eyes did not correlate with the severity of latency delay in the affected eyes（R^2〈0.02, P=0.3）. The differences between ON patients with and without MS, reported here, suggest that the presence of disseminated disease plays critical role in latency delay of the fellow eye.

关键词： multi-focal visual evoked potential optic neuritis fellow eyes latency delay

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