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Absence of galectin-3 promotes neuroprotection in retinal ganglion cells after optic nerve injury

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dc.contributor.authorAbreu, Carla Andreia
dc.contributor.authorDe Lima, Silmara Veline
dc.contributor.authorMendonça, Henrique Rocha
dc.contributor.authorOliveira Goulart, Camila de
dc.contributor.authorBlanco Martinez, Ana Maria
dc.date.accessioned2022-02-15T09:50:35Z
dc.date.available2022-02-15T09:50:35Z
dc.date.issued2017
dc.description.abstractA trauma to the mature central nervous system (CNS) often leads to persistent deficits, due to the inability of axons to regenerate after being injured. Increasing evidence suggests that pro-inflammatory and pro-apoptotic genes can present a major obstacle to promoting neuroprotection of retinal ganglion cells and consequently succeed in axonal regeneration. This study evaluated the effect of the absence of galectin-3 (Gal-3) on retinal ganglion cells (RGC) survival and axonal regeneration/degeneration after optic nerve crush injury. Two weeks after crush there was a 2.6 fold increase in the rate of cell survival in Gal-3-/- mice (1283±79.15) compared to WT animals (495.4±53.96). However, no regeneration was observed in the Gal-3-/- mice two weeks after lesion. Furthermore, axonal degeneration presented a particular pattern on those mice; Electron Microscopy (EM) analysis showed incomplete axon degeneration while the WT mice presented an advanced stage of degeneration. This suggests that the removal of the nerve fibers in the Gal 3-/- mice could be deficient and this would cause a delay in the process of Wallerian degeneration once there is a decrease in the number of macrophages/microglia in the nerve. This study demonstrates how the absence of Gal-3 can affect RGC survival and optic nerve regeneration/degeneration after lesion. Our results suggest that the absence of Gal-3 plays an important role in the survival of RGC and thus can be a potential target for therapeutic intervention in RGC neuroprotection.es
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dc.format.extent10es
dc.identifier.citationHistology and Histopathology, Vol.32, nº3, (2017)
dc.identifier.doiDOI: 10.14670/HH-11-788
dc.identifier.issn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/117026
dc.languageenges
dc.publisherUniversidad de Murcia. Departamento de Biología Celular e Histologíaes
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectRetinal ganglion cellses
dc.subjectOptic nervees
dc.subjectGalectin-3es
dc.subjectWallerian Degenerationes
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes
dc.titleAbsence of galectin-3 promotes neuroprotection in retinal ganglion cells after optic nerve injuryes
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.32, nº3 (2017)