Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7422
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dc.contributor.authorWilding, Corina-
dc.contributor.authorBell, Katharina-
dc.contributor.authorBeck, Sabine-
dc.contributor.authorFunke, Sebastian-
dc.contributor.authorPfeiffer, Norbert-
dc.contributor.authorGrus, Franz-Hermann-
dc.date.accessioned2022-07-14T08:34:23Z-
dc.date.available2022-07-14T08:34:23Z-
dc.date.issued2014
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/7436-
dc.description.abstractThe family of synuclein proteins (alpha, beta and gamma) are related to neurodegenerative disease e.g. Parkinson disease and Morbus Alzheimer. Additionally, a connection between gamma-synuclein and glaucoma, a neurodegenerative disease characterized by a progressive loss of retinal ganglion cells, which finally leads to blindness, exists. The reason for the development of glaucoma is still unknown. Recent studies evaluating the participation of immunological components, demonstrate complex changed antibody reactivities in glaucoma patients in comparison to healthy people, showing not only up-regulations (e.g. alpha-fodrin antibody) but also down-regulations (e.g. gamma-synuclein antibody) of antibodies in glaucoma patients. Up-regulated antibodies could be auto-aggressive, but the role of down-regulated antibodies is still unclear. Previous studies show a significant influence of the serum and the antibodies of glaucoma patients on protein expression profiles of neuroretinal cells. The aim of this study was to investigate the effect of gamma-synuclein antibody on the viability and reactive oxygen species levels of a neuroretinal cell line (RGC-5) as well as their interaction with cellular proteins. We found a protective effect of gamma-synuclein antibody resulting in an increased viability (up to 15%) and decreased reactive oxygen species levels (up to -12%) of glutamate and oxidative stressed RGC-5. These can be traced back to anti-apoptotic altered protein expressions in the mitochondrial apoptosis pathway indicated by mass spectrometry and validated by microarray analysis such as active caspase 3, bcl-2 associated-x-protein, S100A4, voltage-dependent anion channel, extracellular-signal-regulated-kinase (down-regulated) and baculoviral IAP repeat-containing protein 6, phosphorylated extracellular-signal-regulated-kinase (up-regulated). These changed protein expression are triggered by the gamma-synuclein antibody internalization of RGC-5 we could see in immunohistochemical stainings. These findings let us assume a novel physiological function of gamma-synuclein antibodies and give insights in the role of autoantibodies in glaucoma. We hypothesize that the down-regulation of autoantibodies found in glaucoma patients lead to a loss of protective autoimmunity.en_GB
dc.description.sponsorshipDFG, Open Access-Publizieren Universität Mainz / Universitätsmedizinde
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titlegamma-Synuclein antibodies have neuroprotective potential on neuroretinal cells via proteins of the mitochondrial apoptosis pathwayen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-7422-
jgu.type.dinitypearticleen_GB
jgu.type.versionPublished versionde
jgu.type.resourceTextde
jgu.organisation.departmentFB 04 Medizinde
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titlePLoS onede
jgu.journal.volume9de
jgu.journal.issue3de
jgu.pages.alternativee90737de
jgu.publisher.year2014-
jgu.publisher.namePLoSde
jgu.publisher.placeLawrence, Kan.de
jgu.publisher.urihttp://dx.doi.org/10.1371/journal.pone.0090737de
jgu.publisher.issn1932-6203de
jgu.organisation.placeMainz-
jgu.identifier.pmid24595072
jgu.subject.ddccode610de
opus.date.modified2018-08-08T08:46:18Z
opus.subject.dfgcode00-000
opus.organisation.stringFB 04: Medizin: Augenklinik und Poliklinikde_DE
opus.identifier.opusid27339
opus.importsourcepubmed
opus.institute.number0446
opus.metadataonlyfalse
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_EN
opus.affiliatedPfeiffer, Norbert
opus.affiliatedGrus, Franz-Hermann
jgu.publisher.doi10.1371/journal.pone.0090737de
jgu.organisation.rorhttps://ror.org/023b0x485-
Appears in collections:DFG-OA-Publizieren (2012 - 2017)

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