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dc.contributor.authorRuzafa Andrés, Noelia ORCID
dc.contributor.authorRey Santano, María Carmen
dc.contributor.authorMielgo, Victoria
dc.contributor.authorPereiro Díez, Xandra ORCID
dc.contributor.authorVecino Cordero, Elena ORCID
dc.date.accessioned2019-05-06T07:41:07Z
dc.date.available2019-05-06T07:41:07Z
dc.date.issued2017-04-13
dc.identifier.citationPlos One 12(4) : (2017) // Article ID e0175301es_ES
dc.identifier.issn1932-6203
dc.identifier.urihttp://hdl.handle.net/10810/32645
dc.description.abstractPurpose To evaluate the effect of hypoxia on the neonatal pig retina and brain, we analysed the retinal ganglion cells (RGCs) and neurons in the superior colliculus, as well as the response of astrocytes in both these central nervous system (CNS) structures. Methods Newborn pigs were exposed to 120 minutes of hypoxia, induced by decreasing the inspiratory oxygen fraction (FiO(2): 10-15%), followed by a reoxygenation period of 240 minutes (FiO(2): 21-35%). RGCs were quantified using Brn3a, a specific nuclear marker for these cells, and apoptosis was assessed through the appearance of active caspase-3. A morphometric analysis of the cytoskeleton of astrocytes (identified with GFAP) was performed in both the retina and superior colliculus. Results Hypoxia produced no significant change in the RGCs, although, it did induce a 37.63% increase in the number of active caspase-3 positive cells in the superior colliculus. This increase was particularly evident in the superficial layers of the superior colliculus, where 56.93% of the cells were positive for active caspase-3. In addition, hypoxia induced changes in the morphology of the astrocytes in the superior colliculus but not in the retina. Conclusions Hypoxia in the neonatal pig does not affect the retina but it does affect more central structures in the brain, increasing the number of apoptotic cells in the superior colliculus and inducing changes in astrocyte morphology. This distinct sensibility to hypoxia may pave the way to design specific approaches to combat the effects of hypoxia in specific areas of the CNS.es_ES
dc.description.sponsorshipWe acknowledge the support of Retos-MINECO Fondos Fender (RTC-2016-48231) and Grupos Consolidados del Gobierno Vasco (IT43710) to E.V.es_ES
dc.language.isoenges_ES
dc.publisherPublic LIbrary Sciencees_ES
dc.relationinfo:eu-repo/grantAgreement/MINECO/RTC-2016-48231es_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.subjectganglion-cell deathes_ES
dc.subjectoxygen-induced retinopathyes_ES
dc.subjectcentral-nervous-systemes_ES
dc.subjectintraocular-pressurees_ES
dc.subjectmuller cellses_ES
dc.subjectdiabetic-retinopathyes_ES
dc.subjectreactive astrocyteses_ES
dc.subjectoptic tectumes_ES
dc.subjectrat retinaes_ES
dc.subjectbraines_ES
dc.titleEffect of Hypoxia on the Retina and Superior Colliculus of Neonatal Pigses_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.rights.holderThis is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Attribution 4.0 International (CC BY 4.0)es_ES
dc.rights.holderAtribución 3.0 España*
dc.relation.publisherversionhttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0175301es_ES
dc.identifier.doi10.1371/journal.pone.0175301
dc.departamentoesBiología celular e histologíaes_ES
dc.departamentoeuZelulen biologia eta histologiaes_ES


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This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Attribution 4.0 International (CC BY 4.0)
Except where otherwise noted, this item's license is described as This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Attribution 4.0 International (CC BY 4.0)