Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7578
Full metadata record
DC FieldValueLanguage
dc.contributor.authorTeister, Julia-
dc.contributor.authorAnders, F.-
dc.contributor.authorBeck, Sabine-
dc.contributor.authorFunke, S.-
dc.contributor.authorPein, H. von-
dc.contributor.authorProkosch-Willing, Verena-
dc.contributor.authorPfeiffer, Norbert-
dc.contributor.authorGrus, Franz-Hermann-
dc.date.accessioned2022-08-19T10:03:26Z-
dc.date.available2022-08-19T10:03:26Z-
dc.date.issued2017
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/7592-
dc.description.abstractAlthough elevated intraocular pressure (IOP) remains the major risk factor in glaucoma, neurodegenerative processes continue despite effective IOP lowering. Altered α-synuclein antibody (Abs) levels have been reported to play a crucial role. This study aimed at identifying whether α-synuclein Abs are capable to decelerate neuronal decay while providing insights into proteomic changes. Four groups of Sprague Dawley rats received episcleral vein occlusion: (1) CTRL, no intravitreal injection, n = 6, (2) CTRL IgG, intravitreal injection of unspecific IgG, n = 5, (3) Buffer, intravitreal injection of buffer, n = 6, (4), α-synuclein Ab, intravitreal injection of α-synuclein Ab, n = 5. IOP and retinal nerve fiber layer thickness (RNFLT) were monitored and immunohistochemistry, microarray and proteomic analysis were performed. RNFLT was reduced in CTRL, CTRL IgG and Buffer group (all p < 0.01) and α-synuclein Ab group (p = 0.17). Axon and RGC density showed an increased neurodegeneration in CTRL, CTRL IgG and Buffer group (all p < 0.01) and increased neuronal survival in α-synuclein Ab group (p = 0.38 and 0.06, respectively) compared with fellow eyes. Proteomic analysis revealed alterations of cofilin 1 and superoxide dismutase 1 expression. This data indicate that α-synuclein Ab might indirectly modulate the actin cytoskeleton organization and negatively regulate apoptotic processes via cofilin 1 and superoxide dismutase 1.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.titleDecelerated neurodegeneration after intravitreal injection of α-synuclein antibodies in a glaucoma animal modelen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-7578-
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.titleScientific reportsde
jgu.journal.volume7de
jgu.journal.issue1de
jgu.pages.alternativeArt. 6260de
jgu.publisher.year2017-
jgu.publisher.nameMacmillan Publishers Limited, part of Springer Naturede
jgu.publisher.placeLondonde
jgu.publisher.urihttp://dx.doi.org/10.1038/s41598-017-06702-1de
jgu.publisher.issn2045-2322de
jgu.notes.publicProkosch-Willing, Verena veröffentlicht unter: Prokosch, Verenade
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
opus.date.modified2018-04-05T08:06:40Z
opus.subject.dfgcode00-000
opus.organisation.stringFB 04: Medizin: Augenklinik und Poliklinikde_DE
opus.identifier.opusid57967
opus.institute.number0446
opus.metadataonlyfalse
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_EN
opus.affiliatedProkosch-Willing, Verena
opus.affiliatedPfeiffer, Norbert
opus.affiliatedGrus, Franz-Hermann
jgu.publisher.doi10.1038/s41598-017-06702-1de
jgu.organisation.rorhttps://ror.org/023b0x485-
Appears in collections:DFG-OA-Publizieren (2012 - 2017)

Files in This Item:
  File Description SizeFormat
Thumbnail
decelerated_neurodegeneration-20220817163444959.pdf6.54 MBAdobe PDFView/Open