Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7353
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dc.contributor.authorLiu, Hanhan-
dc.contributor.authorAnders, Fabian-
dc.contributor.authorThanos, Solon-
dc.contributor.authorMann, Carolina-
dc.contributor.authorLiu, Aiwei-
dc.contributor.authorGrus, Franz-Hermann-
dc.contributor.authorPfeiffer, Norbert-
dc.contributor.authorProkosch-Willing, Verena-
dc.date.accessioned2022-07-11T10:31:02Z-
dc.date.available2022-07-11T10:31:02Z-
dc.date.issued2017-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/7367-
dc.description.abstractPurpose: Hydrogen sulfide (H2S) is recognized as a novel third signaling molecule and gaseous neurotransmitter. Recently, cell protective properties within the central nervous and cardiovascular system have been proposed. Our purpose was to analyze the expression and neuroprotective effects of H2S in experimental models of glaucoma. Methods: Elevated IOP was induced in Sprague-Dawley rats by means of episcleral vein cauterization. After 7 weeks, animals were killed and the retina was analyzed with label-free mass spectrometry. In vitro, retinal explants were exposed to elevated hydrostatic pressure or oxidative stress (H2O2), with and without addition of a slow-releasing H2S donor Morpholin-4-ium-methoxyphenyl-morpholino-phosphinodithioate (GYY4137). In vivo, GYY4137 was injected intravitreally in animals with acute ischemic injury or optic nerve crush. Brn3a+ retinal ganglion cells (RGCs) were counted in retinal flat mounts and compared. Optical coherence tomography (OCT) was performed to examine the vessels. Comparisons were made by t-test and ANOVA (P < 0.05). Results: IOP elevation caused significant RGC loss (P < 0.001); 3-mercaptosulfurtransferase, an H2S producing enzyme, showed a 3-fold upregulation within the retina after IOP elevation. GYY4137 protected RGCs against elevated pressure and oxidative stress in vitro depending on the concentration used (P < 0.005). In vivo, intravitreal administration of GYY4137 preserved RGCs from acute ischemic injury and optic nerve crush (P < 0.0001). Retinal vessel diameters enlarged after intravitreal GYY4137 injection (P < 0.0001). Conclusions: H2S is specifically regulated in experimental glaucoma. By scavenging reactive oxygen species and dilating retinal vessels, H2S may protect RGCs from pressure and oxidative stress–induced RGC loss in vitro and in vivo. Therefore, H2S might be a novel neuroprotectant in glaucoma.en_GB
dc.description.sponsorshipDFG, Open Access-Publizieren Universität Mainz / Universitätsmedizinde
dc.language.isoengde
dc.rightsCC BY-NC-ND*
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleHydrogen sulfide protects retinal ganglion cells against glaucomatous injury in vitro and in vivoen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-7353-
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.titleInvestigative ophthalmology & visual sciencede
jgu.journal.volume58de
jgu.journal.issue12de
jgu.pages.start5129de
jgu.pages.end5141de
jgu.publisher.year2017-
jgu.publisher.nameARVOde
jgu.publisher.placeRockville, Md.de
jgu.publisher.urihttp://dx.doi.org/10.1167/iovs.17-22200de
jgu.publisher.issn1552-5783de
jgu.publisher.issn0146-0404de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
opus.date.modified2018-03-16T10:12:31Z-
opus.subject.dfgcode00-000-
opus.organisation.stringFB 04: Medizin: Augenklinik und Poliklinikde_DE
opus.identifier.opusid57987-
opus.institute.number0446-
opus.metadataonlyfalse-
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_EN
opus.affiliatedGrus, Franz-Hermann-
opus.affiliatedPfeiffer, Norbert-
opus.affiliatedProkosch-Willing, Verena-
jgu.publisher.doi10.1167/iovs.17-22200de
jgu.organisation.rorhttps://ror.org/023b0x485
Appears in collections:DFG-OA-Publizieren (2012 - 2017)

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