Neuroprotective Effects of Fingolimod in a Cellular Model of Optic Neuritis

Visual dysfunction resulting from optic neuritis (ON) is one of the most common clinical manifestations of multiple sclerosis (MS), characterized by loss of retinal ganglion cells, thinning of the nerve fiber layer, and inflammation to the optic nerve. Current treatments available for ON or MS are o...

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Autores principales:	Amritha A. Candadai, Fang Liu, Arti Verma, Mir S. Adil, Moaddey Alfarhan, Susan C. Fagan, Payaningal R. Somanath, S. Priya Narayanan
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	optic neuritis multiple sclerosis oxidative stress neuroprotection fingolimod Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/84d2577ff1f94fce89aef8faa6029b1e
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spelling	oai:doaj.org-article:84d2577ff1f94fce89aef8faa6029b1e2021-11-25T17:09:22ZNeuroprotective Effects of Fingolimod in a Cellular Model of Optic Neuritis10.3390/cells101129382073-4409https://doaj.org/article/84d2577ff1f94fce89aef8faa6029b1e2021-10-01T00:00:00Zhttps://www.mdpi.com/2073-4409/10/11/2938https://doaj.org/toc/2073-4409Visual dysfunction resulting from optic neuritis (ON) is one of the most common clinical manifestations of multiple sclerosis (MS), characterized by loss of retinal ganglion cells, thinning of the nerve fiber layer, and inflammation to the optic nerve. Current treatments available for ON or MS are only partially effective, specifically target the inflammatory phase, and have limited effects on long-term disability. Fingolimod (FTY) is an FDA-approved immunomodulatory agent for MS therapy. The objective of the current study was to evaluate the neuroprotective properties of FTY in the cellular model of ON-associated neuronal damage. R28 retinal neuronal cell damage was induced through treatment with tumor necrosis factor-α (TNFα). In our cell viability analysis, FTY treatment showed significantly reduced TNFα-induced neuronal death. Treatment with FTY attenuated the TNFα-induced changes in cell survival and cell stress signaling molecules. Furthermore, immunofluorescence studies performed using various markers indicated that FTY treatment protects the R28 cells against the TNFα-induced neurodegenerative changes by suppressing reactive oxygen species generation and promoting the expression of neuronal markers. In conclusion, our study suggests neuroprotective effects of FTY in an in vitro model of optic neuritis.Amritha A. CandadaiFang LiuArti VermaMir S. AdilMoaddey AlfarhanSusan C. FaganPayaningal R. SomanathS. Priya NarayananMDPI AGarticleoptic neuritismultiple sclerosisoxidative stressneuroprotectionfingolimodBiology (General)QH301-705.5ENCells, Vol 10, Iss 2938, p 2938 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	optic neuritis multiple sclerosis oxidative stress neuroprotection fingolimod Biology (General) QH301-705.5
spellingShingle	optic neuritis multiple sclerosis oxidative stress neuroprotection fingolimod Biology (General) QH301-705.5 Amritha A. Candadai Fang Liu Arti Verma Mir S. Adil Moaddey Alfarhan Susan C. Fagan Payaningal R. Somanath S. Priya Narayanan Neuroprotective Effects of Fingolimod in a Cellular Model of Optic Neuritis
description	Visual dysfunction resulting from optic neuritis (ON) is one of the most common clinical manifestations of multiple sclerosis (MS), characterized by loss of retinal ganglion cells, thinning of the nerve fiber layer, and inflammation to the optic nerve. Current treatments available for ON or MS are only partially effective, specifically target the inflammatory phase, and have limited effects on long-term disability. Fingolimod (FTY) is an FDA-approved immunomodulatory agent for MS therapy. The objective of the current study was to evaluate the neuroprotective properties of FTY in the cellular model of ON-associated neuronal damage. R28 retinal neuronal cell damage was induced through treatment with tumor necrosis factor-α (TNFα). In our cell viability analysis, FTY treatment showed significantly reduced TNFα-induced neuronal death. Treatment with FTY attenuated the TNFα-induced changes in cell survival and cell stress signaling molecules. Furthermore, immunofluorescence studies performed using various markers indicated that FTY treatment protects the R28 cells against the TNFα-induced neurodegenerative changes by suppressing reactive oxygen species generation and promoting the expression of neuronal markers. In conclusion, our study suggests neuroprotective effects of FTY in an in vitro model of optic neuritis.
format	article
author	Amritha A. Candadai Fang Liu Arti Verma Mir S. Adil Moaddey Alfarhan Susan C. Fagan Payaningal R. Somanath S. Priya Narayanan
author_facet	Amritha A. Candadai Fang Liu Arti Verma Mir S. Adil Moaddey Alfarhan Susan C. Fagan Payaningal R. Somanath S. Priya Narayanan
author_sort	Amritha A. Candadai
title	Neuroprotective Effects of Fingolimod in a Cellular Model of Optic Neuritis
title_short	Neuroprotective Effects of Fingolimod in a Cellular Model of Optic Neuritis
title_full	Neuroprotective Effects of Fingolimod in a Cellular Model of Optic Neuritis
title_fullStr	Neuroprotective Effects of Fingolimod in a Cellular Model of Optic Neuritis
title_full_unstemmed	Neuroprotective Effects of Fingolimod in a Cellular Model of Optic Neuritis
title_sort	neuroprotective effects of fingolimod in a cellular model of optic neuritis
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/84d2577ff1f94fce89aef8faa6029b1e
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Neuroprotective Effects of Fingolimod in a Cellular Model of Optic Neuritis

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