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dc.contributor.authorAlonso Alconada, Daniel ORCID
dc.date.accessioned2022-06-08T11:39:23Z
dc.date.available2022-06-08T11:39:23Z
dc.date.issued2022-04-28
dc.identifier.citationFrontiers in Pediatrics 10 : (2022) // Article ID 793189es_ES
dc.identifier.urihttp://hdl.handle.net/10810/56852
dc.description.abstractCellular and tissue damage triggered after hypoxia-ischemia (HI) can be generalized and affect the neurogenic niches present in the central nervous system. As neuroregeneration may be critical for optimizing functional recovery in neonatal encephalopathy, the goal of the present work was to investigate the neurogenic response to HI in the neurogenic niche of the subventricular zone (SVZ) in the neonatal piglet. A total of 13 large white male piglets aged <24 h were randomized into two groups: i) HI group (n = 7), animals submitted to transient cerebral HI and resuscitation; and ii) Control group (n = 6), non-HI animals. At 48 h, piglets were euthanized, and the SVZ and its surrounding regions, such as caudate and periventricular white matter, were analyzed for histology using hematoxylin-eosin staining and immunohistochemistry by evaluating the presence of cleaved caspase 3 and TUNEL positive cells, together with the cell proliferation/neurogenesis markers Ki67 (cell proliferation), GFAP (neural stem cells processes), Sox2 (neural stem/progenitor cells), and doublecortin (DCX, a marker of immature migrating neuroblasts). Hypoxic-ischemic piglets showed a decrease in cellularity in the SVZ independent of cell death, together with decreased length of neural stem cells processes, neuroblast chains area, DCX immunoreactivity, and lower number of Ki67 + and Ki67 + Sox2 + cells. These data suggest a reduction in both cell proliferation and neurogenesis in the SVZ of the neonatal piglet, which could in turn compromise the replacement of the lost neurons and the achievement of global repair.es_ES
dc.description.sponsorshipThis work was supported by the United Kingdom Medical Research Council (G0501259), Basque Government Postdoctoral Program (POS_2013_1_191), EITB Maratoia- BIOEF (BIO18/IC/003), and the Spanish Ministry of Science and Innovation (MINECOR20/P66/AEI/10.13039/50110001103). This study was undertaken at University College London Hospitals/University College London, which received a proportion of funding from the UK Department of Health’s National Institute for Health Research Biomedical Research Centers funding scheme.es_ES
dc.language.isoenges_ES
dc.publisherFrontiers Mediaes_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.subjectnewbornes_ES
dc.subjectneonatal braines_ES
dc.subjecthypoxia-ischemiaes_ES
dc.subjectneurogenesises_ES
dc.subjectsubventricular zonees_ES
dc.subjectregenerative capacityes_ES
dc.subjectcaspase activationes_ES
dc.subjectdentate gyruses_ES
dc.subjectprogenitorses_ES
dc.subjectinjuryes_ES
dc.subjectproliferationes_ES
dc.subjectdoublees_ES
dc.subjectcortines_ES
dc.subjectneuronses_ES
dc.subjectgrowthes_ES
dc.titleNeurogenesis Is Reduced at 48 h in the Subventricular Zone Independent of Cell Death in a Piglet Model of Perinatal Hypoxia-Ischemiaes_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.rights.holder022 Alonso-Alconada, Gressens, Golay and Robertson. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.es_ES
dc.rights.holderAtribución 3.0 España*
dc.relation.publisherversionhttps://www.frontiersin.org/articles/10.3389/fped.2022.793189/fulles_ES
dc.identifier.doi10.3389/fped.2022.79318
dc.departamentoesBiología celular e histologíaes_ES
dc.departamentoeuZelulen biologia eta histologiaes_ES


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022 Alonso-Alconada, Gressens, Golay and Robertson. This is an
open-access article distributed under the terms of the Creative Commons Attribution
License (CC BY). The use, distribution or reproduction in other forums is permitted,
provided the original author(s) and the copyright owner(s) are credited and that the
original publication in this journal is cited, in accordance with accepted academic
practice. No use, distribution or reproduction is permitted which does not comply
with these terms.
Except where otherwise noted, this item's license is described as 022 Alonso-Alconada, Gressens, Golay and Robertson. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.