Thioredoxin 1 and glutaredoxin 2 contribute to maintain the phenotype and integrity of neurons following perinatal asphyxia

Romero, Juan Ignacio; Hanschmann, Eva-Maria; Gellert, Manuela; Eitner, Susanne; Holubiec, Mariana; Calvo, Eduardo Blanco; Lillig, Christopher Horst; Capani, Francisco

doi:10.1016/j.bbagen.2015.02.015

Cited by 25 publications

(44 citation statements)

References 104 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The model for common carotid artery ligation used in this study has been previously developed and validated [23, 25]. P7 male Sprague-Dawley rats were anesthetized (40 mg/kg ketamine and 4 mg/kg xylazine) and placed on a heat plate to keep their body temperature at constant 37°C.…”

Section: Methodsmentioning

confidence: 99%

“…Western blot analysis was performed as previously described in Romero et al [23]. Animals were euthanized by decapitation, and brains were dissected, homogenized in ice-cold lysis buffer (10 mM Tris/HCl, pH 7.4, 10 mM NaCl, 3 mM MgCl 2 , 0.1% NP-40, protease inhibitors), and fast frozen in liquid nitrogen.…”

Section: Methodsmentioning

confidence: 99%

“…Particularly, both Grx2 and Trx1 seem to protect neuronal cells from hypoxia-induced damage, while Trx1 knock-down decreases cellular proliferation and viability. Moreover, the absence of either Grx2 or Trx1 following hypoxia and reoxygenation triggers differentiation into a glial-like cell type [23]. Interestingly, it was shown before in zebra fish that the loss of glutaredoxin leads to neuronal apoptosis and loss of an axonal scaffold, making Grx an essential protein for embryonic brain development [24].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Neuronal Damage Induced by Perinatal Asphyxia Is Attenuated by Postinjury Glutaredoxin‐2 Administration

Romero

Holubiec

Tornatore

et al. 2017

Oxidative Medicine and Cellular Longevity

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Neuronal Damage Induced by Perinatal Asphyxia Is Attenuated by Postinjury Glutaredoxin‐2 Administration

Romero

Holubiec

Tornatore

et al. 2017

Oxidative Medicine and Cellular Longevity

Self Cite

View full text Add to dashboard Cite

show abstract

“…The Swedish experimental model of PA appears to be a useful tool of clinical relevance [26, 30, 33, 34, 54–56]. Also electrophysiological evidence is needed so as to clarify the relevance of new dysfunctional synapses and long-term neurodegeneration leading to synaptopathy following PA.…”

Section: Discussionmentioning

confidence: 99%

“…It resembles normal labour minimizing the influence of surgery, anesthesia, or drugs [30]. The main advantages of this model can be summarized as follows: (a) asphyxia takes place at the time of the delivery much the same as when umbilical cord circulation is disrupted; (b) the procedure results in systemic acidosis, hypercapnia, and hypoxia as observed in global asphyxia; (c) it is not invasive avoiding the confounding interferences of surgical procedures; (d) it induces global asphyxia which affects the whole brain (cerebral hemispheres and deep structures) making the model suitable for behavioural studies [26, 33, 34]. …”

Section: Experimental Model Of Perinatal Asphyxia: Early Damage Inmentioning

confidence: 99%

Could Perinatal Asphyxia Induce a Synaptopathy? New Highlights from an Experimental Model

et al. 2017

Self Cite

View full text Add to dashboard Cite

Birth asphyxia also termed perinatal asphyxia is an obstetric complication that strongly affects brain structure and function. Central nervous system is highly susceptible to oxidative damage caused by perinatal asphyxia while activation and maturity of the proper pathways are relevant to avoiding abnormal neural development. Perinatal asphyxia is associated with high morbimortality in term and preterm neonates. Although several studies have demonstrated a variety of biochemical and molecular pathways involved in perinatal asphyxia physiopathology, little is known about the synaptic alterations induced by perinatal asphyxia. Nearly 25% of the newborns who survive perinatal asphyxia develop neurological disorders such as cerebral palsy and certain neurodevelopmental and learning disabilities where synaptic connectivity disturbances may be involved. Accordingly, here we review and discuss the association of possible synaptic dysfunction with perinatal asphyxia on the basis of updated evidence from an experimental model.

show abstract

Noise‐induced hippocampal oxidative imbalance and aminoacidergic neurotransmitters alterations in developing male rats: Influence of enriched environment during adolescence

Molina

Buján

Guelman

2021

Developmental Neurobiology

View full text Add to dashboard Cite

Living in big cities might involuntarily expose people to high levels of noise causing auditory and/or extra‐auditory impairments, including adverse effects on central nervous system (CNS) areas such as the hippocampus. In particular, CNS development is a very complex process that can be altered by environmental stimuli. We have previously shown that noise exposure of developing rats can induce hippocampal‐related behavioral alterations. However, noise‐induced biochemical alterations had not been studied yet. Thus, the aim of this work was to assess whether early noise exposure can affect rat hippocampal oxidative state and aminoacidergic neurotransmission tone. Additionally, the effectiveness of an enriched environment (EE) as a neuroprotective strategy was evaluated. Male Wistar rats were exposed to different noise schemes at 7 or 15 days after birth. Upon weaning, some animals were transferred to an EE whereas others were kept in standard cages. Short‐ and long‐term measurements were performed to evaluate reactive oxygen species, thioredoxins levels and catalase activity as indicators of hippocampal oxidative status as well as glutamic acid decarboxylase and a subtype of glutamate transporter to evaluate aminoacidergic neurotransmission tone. Results showed noise‐induced changes in hippocampal oxidative state and aminoacidergic neurotransmission markers that lasted until adolescence and differed according to the scheme and the age of exposure. Finally, EE housing was effective in preventing some of these changes. These findings suggest that CNS development seems to be sensitive to the effects of stressors such as noise, as well as those of an environmental stimulation, favoring prompt and lasting molecular changes.

show abstract

Thioredoxin 1 and glutaredoxin 2 contribute to maintain the phenotype and integrity of neurons following perinatal asphyxia

Cited by 25 publications

References 104 publications

Neuronal Damage Induced by Perinatal Asphyxia Is Attenuated by Postinjury Glutaredoxin‐2 Administration

Neuronal Damage Induced by Perinatal Asphyxia Is Attenuated by Postinjury Glutaredoxin‐2 Administration

Could Perinatal Asphyxia Induce a Synaptopathy? New Highlights from an Experimental Model

Noise‐induced hippocampal oxidative imbalance and aminoacidergic neurotransmitters alterations in developing male rats: Influence of enriched environment during adolescence

Contact Info

Product

Resources

About