Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7428
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dc.contributor.authorGramlich, Oliver W.-
dc.contributor.authorTeister, Julia-
dc.contributor.authorNeumann, Mareike-
dc.contributor.authorTao, Xue-
dc.contributor.authorBeck, Sabine-
dc.contributor.authorPein, Harald von-
dc.contributor.authorPfeiffer, Norbert-
dc.contributor.authorGrus, Franz-Hermann-
dc.date.accessioned2022-07-15T07:34:00Z-
dc.date.available2022-07-15T07:34:00Z-
dc.date.issued2016
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/7442-
dc.description.abstractBACKGROUND: Elevated intraocular pressure (IOP), as well as fluctuations in IOP, is a main risk factor for glaucoma, but its pathogenic effect has not yet been clarified. Beyond the multifactorial pathology of the disease, autoimmune mechanisms seem to be linked to retinal ganglion cell (RGC) death. This study aimed to identify if intermittent IOP elevations in vivo (i) elicit neurodegeneration, (ii) provokes an immune response and (iii) whether progression of RGC loss can be attenuated by the B lymphocyte inhibitor Belimumab. METHODS: Using an intermittent ocular hypertension model (iOHT), Long Evans rats (n = 21) underwent 27 unilateral simulations of a fluctuating pressure profile. Nine of these animals received Belimumab, and additional seven rats served as normotensive controls. Axonal density was analyzed in PPD-stained optic nerve cross-sections. Retinal cross-sections were immunostained against Brn3a, Iba1, and IgG autoantibody depositions. Serum IgG concentration and IgG reactivities were determined using ELISA and protein microarrays. Data was analyzed using ANOVA and Tukey HSD test (unequal N) or student’s independent t test by groups. RESULTS: A wavelike IOP profile led to a significant neurodegeneration of optic nerve axons (−10.6 %, p < 0.001) and RGC (−19.5 %, p = 0.02) in iOHT eyes compared with fellow eyes. Belimumab-treated animals only showed slightly higher axonal survival and reduced serum IgG concentration (−29 %) after iOHT. Neuroinflammatory events, indicated by significantly upregulated microglia activation and IgG autoantibody depositions, were shown in all injured retinas. Significantly elevated serum autoantibody immunoreactivities against glutathione-S-transferase, spectrin, and transferrin were observed after iOHT and were negatively correlated to the axon density. CONCLUSIONS: Intermittent IOP elevations are sufficient to provoke neurodegeneration in the optic nerve and the retina and elicit changes of IgG autoantibody reactivities. Although the inhibition of B lymphocyte activation failed to ameliorate axonal survival, the correlation between damage and changes in the autoantibody reactivity suggests that autoantibody profiling could be useful as a biomarker for glaucoma.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.titleImmune response after intermittent minimally invasive intraocular pressure elevations in an experimental animal model of glaucomaen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-7428-
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.titleJournal of neuroinflammationde
jgu.journal.volume13de
jgu.pages.alternativeArt. 82de
jgu.publisher.year2016-
jgu.publisher.nameBioMed Centralde
jgu.publisher.placeLondonde
jgu.publisher.urihttp://dx.doi.org/10.1186/s12974-016-0542-6de
jgu.publisher.issn1742-2094de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
opus.date.modified2018-08-23T08:21:22Z
opus.subject.dfgcode00-000
opus.organisation.stringFB 04: Medizin: Institut für Pathologiede_DE
opus.organisation.stringFB 04: Medizin: Augenklinik und Poliklinikde_DE
opus.identifier.opusid56320
opus.institute.number0423
opus.institute.number0446
opus.metadataonlyfalse
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_EN
opus.affiliatedPein, Harald von
opus.affiliatedPfeiffer, Norbert
opus.affiliatedGrus, Franz-Hermann
jgu.publisher.doi10.1186/s12974-016-0542-6de
jgu.organisation.rorhttps://ror.org/023b0x485-
Appears in collections:DFG-OA-Publizieren (2012 - 2017)

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