RT Journal Article
T1 Neuronal Damage Induced by Perinatal Asphyxia Is Attenuated by Postinjury Glutaredoxin-2 Administration
A1 Ignacio Romero, Juan
A1 Ines Holubiec, Mariana
A1 Logica Tornatore, Tamara
A1 Riviere, Stephanie
A1 Hanschmann, Eva-Maria
A1 Alberto Kolliker-Frers, Rodolfo
A1 Tau, Julia
A1 Blanco, Eduardo
A1 Galeano, Pablo
A1 Rodriguez de Fonseca, Fernando
A1 Lillig, Christopher Horst
A1 Capani, Francisco
K1 Heat-shock-protein
K1 Cerebellar granule neurons
K1 Dopamine-induced apoptosis
K1 Ischemic brain-damage
K1 Nf-kappa-b
K1 Neurological reflexes
K1 Cerebral-ischemia
K1 Oxidative stress
K1 Mixed disulfide
K1 Redox control
AB 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.
PB Hindawi ltd
SN 1942-0900
YR 2017
FD 2017-01-01
LK http://hdl.handle.net/10668/19057
UL http://hdl.handle.net/10668/19057
LA en
DS RISalud
RD Apr 10, 2025