Siponimod exerts neuroprotective effects on the retina and higher visual pathway through neuronal S1PR1 in experimental glaucoma
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...
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| Vydáno v: | Neural regeneration research Ročník 18; číslo 4; s. 840 - 848 |
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Mumbai
Wolters Kluwer India Pvt. Ltd
01.04.2023
Medknow Publications & Media Pvt. Ltd Department of Clinical Medicine,Faculty of Medicine,Health and Human Sciences,Macquarie University,North Ryde,Sydney,NSW,Australia Wolters Kluwer - Medknow Wolters Kluwer Medknow Publications |
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| ISSN: | 1673-5374, 1876-7958 |
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| Abstract | 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 S1PR1flox/flox mice 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 S1PR1 signaling 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 therapeutic target and its modulation by siponimod has positive implications in glaucoma conditions. |
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| AbstractList | 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 S1PR1flox/flox mice 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 S1PR1 signaling 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 therapeutic target and its modulation by siponimod has positive implications in glaucoma conditions. 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 S1PR1flox/flox mice 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 S1PR1 signaling 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 therapeutic target and its modulation by siponimod has positive implications in glaucoma conditions.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 S1PR1flox/flox mice 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 S1PR1 signaling 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 therapeutic target and its modulation by siponimod has positive implications in glaucoma conditions. |
| Author | Wall, Roshana Graham, Stuart Pushpitha, Kanishka Sharma, Samridhi Rajput, Rashi Mirzaei, Mehdi Chitranshi, Nitin Basavarajappa, Devaraj Klistorner, Alexander Gupta, Vivek |
| AuthorAffiliation | Department of Clinical Medicine,Faculty of Medicine,Health and Human Sciences,Macquarie University,North Ryde,Sydney,NSW,Australia |
| AuthorAffiliation_xml | – name: Department of Clinical Medicine,Faculty of Medicine,Health and Human Sciences,Macquarie University,North Ryde,Sydney,NSW,Australia – name: Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, Australia |
| Author_xml | – sequence: 1 givenname: Devaraj surname: Basavarajappa fullname: Basavarajappa, Devaraj organization: Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW – sequence: 2 givenname: Vivek surname: Gupta fullname: Gupta, Vivek organization: Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW – sequence: 3 givenname: Nitin surname: Chitranshi fullname: Chitranshi, Nitin organization: Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW – sequence: 4 givenname: Roshana surname: Wall fullname: Wall, Roshana organization: Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW – sequence: 5 givenname: Rashi surname: Rajput fullname: Rajput, Rashi organization: Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW – sequence: 6 givenname: Kanishka surname: Pushpitha fullname: Pushpitha, Kanishka organization: Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW – sequence: 7 givenname: Samridhi surname: Sharma fullname: Sharma, Samridhi organization: Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW – sequence: 8 givenname: Mehdi surname: Mirzaei fullname: Mirzaei, Mehdi organization: Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW – sequence: 9 givenname: Alexander surname: Klistorner fullname: Klistorner, Alexander organization: Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW – sequence: 10 givenname: Stuart surname: Graham fullname: Graham, Stuart organization: Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW |
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| Issue | 4 |
| Keywords | intraocular pressure glaucoma neuroprotection neurodegeneration optic nerve injury retinal ganglion cells sphingosine-1-phosphate siponimod |
| Language | English |
| License | http://creativecommons.org/licenses/by-nc-sa/4.0 This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms. |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Author contributions: DB, VG, MM, AK and SLG designed the study; DB, RVW, NC, KP, and RR performed the experiments; DB, VG, and SLG analyzed the data; DB and VG wrote the manuscript; MM, SS helped to write the manuscript. All authors helped to write the manuscript preparation and approved the final version of the manuscript. |
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| PublicationTitle | Neural regeneration research |
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| Publisher | Wolters Kluwer India Pvt. Ltd Medknow Publications & Media Pvt. Ltd Department of Clinical Medicine,Faculty of Medicine,Health and Human Sciences,Macquarie University,North Ryde,Sydney,NSW,Australia Wolters Kluwer - Medknow Wolters Kluwer Medknow Publications |
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| SubjectTerms | Glaucoma glaucoma; intraocular pressure; neurodegeneration; neuroprotection; optic nerve injury; retinal ganglion cells; siponimod; sphingosine-1-phosphate Nervous system Optic nerve Retina |
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| Title | Siponimod exerts neuroprotective effects on the retina and higher visual pathway through neuronal S1PR1 in experimental glaucoma |
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