dc.contributor.author |
Romero, Juan Ignacio |
dc.contributor.author |
Holubiec, Mariana Inés |
dc.contributor.author |
Logica, Tamara |
dc.contributor.author |
Rivière, Stéphanie |
dc.contributor.author |
Hanschmann, Eva Maria |
dc.contributor.author |
Kölliker Frers, Rodolfo |
dc.contributor.author |
Tau, Julia |
dc.contributor.author |
Blanco Calvo, Eduardo |
dc.contributor.author |
Galeano, Pablo |
dc.contributor.author |
Rodríguez de Fonseca, Fernando |
dc.contributor.author |
Horst Lillig, Christopher |
dc.contributor.author |
Capani, Francisco |
dc.date |
2017-11-06T16:43:55Z |
dc.date |
2017-11-06T16:43:55Z |
dc.date |
2017 |
dc.date |
2017-11-06T16:43:55Z |
dc.identifier |
1942-0900 |
dc.identifier |
1942-0994 |
dc.identifier |
http://hdl.handle.net/10459.1/60425 |
dc.identifier |
https://doi.org/10.1155/2017/4162465 |
dc.identifier.uri |
http://hdl.handle.net/10459.1/60425 |
dc.description |
The general disruption of redox signaling following an ischemia-reperfusion episode has been proposed as a crucial component in neuronal death and consequently brain damage. Thioredoxin (Trx) family proteins control redox reactions and ensure protein regulation via specific, oxidative posttranslational modifications as part of cellular signaling processes. Trx proteins function in the manifestation, progression, and recovery following hypoxic/ischemic damage. Here, we analyzed the neuroprotective effects of postinjury, exogenous administration of Grx2 and Trx1 in a neonatal hypoxia/ischemia model. P7 Sprague-Dawley rats were subjected to right common carotid ligation or sham surgery, followed by an exposure to nitrogen. 1 h later, animals were injected i.p. with saline solution, 10 mg/kg recombinant Grx2 or Trx1, and euthanized 72 h postinjury. Results showed that Grx2 administration, and to some extent Trx1, attenuated part of the neuronal damage associated with a perinatal hypoxic/ischemic damage, such as glutamate excitotoxicity, axonal integrity, and astrogliosis. Moreover, these treatments also prevented some of the consequences of the induced neural injury, such as the delay of neurobehavioral development. To our knowledge, this is the first study demonstrating neuroprotective effects of recombinant Trx proteins on the outcome of neonatal hypoxia/ischemia, implying clinical potential as neuroprotective agents that might counteract neonatal hypoxia/ischemia injury. |
dc.format |
application/pdf |
dc.language |
eng |
dc.publisher |
Hindawi Publishing Corporation |
dc.relation |
This work was supported by the Deutsche Forschungsge-meinschaft (SFB593-N01, LI984/3-1, and GRK1947-A1) to Christopher Horst Lillig; the Federal Ministry for Science and Education (BMBF: 01DN13023-PAREDOX) and MINCYT to Christopher Horst Lillig and Francisco Capani; the German Academic Exchange Service DAAD and MINCYT (PROALAR program) to Christopher Horst Lillig and Francisco Capani; the National Scientific and Technical Research Council (PIP 11420100100159, CONICET, Argentina) to Francisco Capani; Instituto de Salud Carlos III, Ministerio de Economía y Competitividad UE/ERDF grants PI16/01698 and Red de Trastornos Adictivos RD16/0017/0001, and Fundació “La Marató deTV3”(Grant no. 386/C/2011) to Fernando Rodríguez de Fonseca; and the University of Buenos Aires (UBACYT 20020090100118) to Francisco Capani. Juan Ignacio Romero, Mariana Inés Holubiec, Stéphanie Rivière, and Tamara Logica Tornatore are fellowship holders from the National Scientific and Technical Research Council (CONICET, Argentina). Francisco Capani and Pablo Galeano are researchers from the National Scientific and Technical Research Council (CONICET, Argentina). Eduardo Blanco is an associate professor of the Serra-Hunter Programme from the Catalan Government. |
dc.relation |
Reproducció del document publicat a: https://doi.org/10.1155/2017/4162465 |
dc.relation |
Oxidative Medicine And Cellular Longevity, 2017, vol. 2017, núm. 4162465, p. 1-14 |
dc.rights |
cc-by (c) Romero, Juan Ignacio et al., 2017 |
dc.rights |
https://creativecommons.org/licenses/by/4.0 |
dc.rights |
info:eu-repo/semantics/openAccess |
dc.subject |
Neurologia |
dc.subject |
Neurology |
dc.title |
Neuronal damage induced by perinatal asphyxia is attenuated by postinjury glutaredoxin-2 administration |
dc.type |
info:eu-repo/semantics/article |
dc.type |
info:eu-repo/semantics/publishedVersion |