Distribution of the thioredoxin family protein in the rat central nervous system. Role in the perinatal asphyxia pathogenesis.

CAPANI, FRANCISCO; AON-BERTOLINO, MARÍA LAURA; ROMERO, JUAN IGNACIO; GALEANO, PABLO; SARACENO, GUSTAVO EZEQUIEL; AYALA, MARÍA VICTORIA; BADORREY, MARÍA SOL; HOLUBIEC, MARIANA INÉS; KÖLLIKER FRERS, RODOLFO ALBERTO; HANSCHMANN, EVA-MARIA; LILLIG, CHRISTOPHER HORST

Florencia

Congreso; 8th IBRO World Congress of Neuroscience; 2011

International Brain Research Organization (IBRO)

Most animal models of hypoxia ischemia in the central nervous system use rats to study the mechanisms involved in neuronal cell death. The oxidoreductases of the thioredoxin family of proteins play an important role in the cellular response to oxidative stress. Redox imbalance is a major feature of brain damage. For instance, neuronal damage and glial reaction induced by a hypoxic ischemic episode is highly related to glutamate excitotoxicity, oxidative stress and mitochondrial dysfunction. However, no comprehensive study on the localization of the redox proteins in the rat CNS is available. The aim of this work is to study the distribution of the following proteins of the thioredoxin and glutathione glutaredoxin systems in the rat CNS by Inmunohistochemistry, Trx1, Trx2, TrxR1, TrxR2, Txnip, Grx1, Grx2, Grx3, Grx5, and gamma-GCS, peroxiredoxin 1, Prx2, Prx3, Prx4, Prx5, and Prx6. We have focused on areas most sensitive to a hypoxia ischemic insult: Cerebellum, striatum, hippocampus, spinal cord, substantia nigra, cortex and retina. Previous studies suggested that these redox proteins may be distributed in most cell types and regions of the CNS. Here, we have observed remarkable differences in both abundance and regional distribution that point to a complex interplay and crosstalk between the proteins of this family. We think that these data might be helpful to reveal new insights into the role of thiol redox pathways in the pathogenesis of perinatal asphyxia and neurodegenerative disorders of the CNS. Supported by UBATYC 20020090100118 CONICET 11420100100159 and DA0810.