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Apoptotic retinal ganglion cell death after optic nerve transection or crush in mice: delayed RGC loss with BDNF or a Caspase 3 inhibitor

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dc.contributor.authorSánchez-Migallón, María C.
dc.contributor.authorValiente Soriano, Francisco Javier
dc.contributor.authorNadal-Nicolás, Francisco Manuel
dc.contributor.authorVidal Sanz, Manuel
dc.contributor.authorAgudo Barriuso, Marta
dc.contributor.departmentOftalmología, Optometría, Otorrinolaringología y Anatomía Patológica
dc.contributor.otherFacultad de Medicina
dc.date.accessioned2026-01-27T18:56:38Z
dc.date.available2026-01-27T18:56:38Z
dc.date.copyright© 2016 The Author(s)
dc.date.issued2016-01
dc.description.abstractPurpose: To investigate retinal ganglion cell (RGC) survival and activation of caspase 3 after optic nerve crush (ONC) or transection (ONT) and treatment with brain-derived neurotrophic factor (BDNF) or Z-DEVD_fmk. Methods: In albino Swiss mice, the left optic nerve was severed or crushed at 0.5 mm from the optic head and retinas were analyzed from 1 to 10 days. Additional groups were treated intravitreally with a single injection of BDNF (2.5 μg) or Z-DEVD_fmk (125 ng) right after injury, or with Z-DEVD_fmk at day 2, or with multiple injections of Z-DEVD_fmk. As controls intact or vehicle-treated retinas were used. In all retinas, Brn3a (RGCs) and cleaved-caspase 3 (c-casp3) were immunodetected and their numbers quantified. In an additional group, c-casp3 expression was assessed in RGCs retrogradely labeled before axotomy. Results: The temporal loss of RGCs was the same after ONC or ONT and occurred in two phases with 65% loss during the first 7 days and an additional 4% loss from day 7 to 10. The appearance of c-casp3+RGCs is Gaussian, peaking at 4 days and declining thereafter. Brn3a down-regulates when RGCs start expressing c-casp3. Retinal ganglion cell rescue rate for BDNF or Z-DEVD_fmk is similar and both delay RGC loss by 1 day. Delayed treatment with Z-DEVD_fmk does not rescue RGCs, and several injections are not better than a single one at the time of the injury. Conclusions: Brn3a down-regulation marks the beginning of RGC death, which after axotomy occurs by caspase-dependent apoptosis in at least half of the RGCs. These data should be considered when designing neuroprotective strategies.
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dc.format.extent13
dc.identifier.citation Invest Ophthal mol Vis Sci. 2016;57:81–93
dc.identifier.doihttps://doi.org/10.1167/iovs.15-17841
dc.identifier.eissn1552-5783
dc.identifier.issn0146-0404
dc.identifier.urihttp://hdl.handle.net/10201/195329
dc.languageeng
dc.publisherAssociation for Research in Vision and Ophthalmology
dc.relationSupported by Spanish Ministry of Economy and Competitiveness Grants SAF-2012-38328 and PI13/00643 and Instituto de Salud Carlos III (ISCIII).
dc.relation.publisherversionhttps://iovs.arvojournals.org/article.aspx?articleid=2482663
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectActive caspase 3
dc.subjectBDNF
dc.subjectZ-DEVD
dc.subjectNeuroprotection
dc.subjectBrn3a
dc.subject.odsObjetivo 3: Salud
dc.titleApoptotic retinal ganglion cell death after optic nerve transection or crush in mice: delayed RGC loss with BDNF or a Caspase 3 inhibitor
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/publishedVersion
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