Neuropharmacology

Biography

Biography: Francisco Capani

Abstract

Thioredoxin (Trx) family proteins are a key mediator for different cell functions via regulation of the thiol redox state of several proteins and the levels of the second messenger hydrogen peroxide. Their modifications have been involved in various pathologies. Then the studied of the role of Trxs in neuronal recovery, following hypoxia/ischemia and reperfusion in both “in vitro” and “in vivo” model of perinatal asphyxia is important to understand the physiopathology of this disease. For that propose we have analyzed the distribution of 14 Trx family proteins in the cerebellum, striatum, and hippocampus. In addition we have perform a set of experiments to dissect the functions of some redoxins as suggested in vivo model of perinatal asphyxia in SH-SY5Y cells subjected to hypoxia and reoxygenation. Using both approaches, we have discovered a cell-type and tissue-specific expression pattern following the hypoxia/ischemia and reoxygenation. Specifically, Grx2 and Trx1 showed a particular deeply modifications during cell tissue recovery. Silencing of these proteins in SH-SY5Y cells subjected to hypoxia-reoxygenation strongly suggested that these proteins are related to maintain the normal neuronal and astrogial phenotype. These data demonstrate the significance of redox signaling in cellular pathways. Grx2 and Trx1 contribute significantly to neuronal integrity and could be clinically relevant in neuronal damage induced by perinatal asphyxia and its neurological deficits including delayed mental and motor development, epilepsy and major cognitive deficits. Therefore, redoxins give a unique opportunity for studying their role as therapeutic tools in a disease that up today does not have any efficient cure.