Characterization of the expression pattern of the thioredoxins protein family in a hypoxic-ischemic rat model

ROMERO, JUAN IGNACIO; GALEANO, PABLO; HANSCHMANN, EVA-MARIA; LILLIG, CHRISTOPHER HORST; CAPANI, FRANCISCO

Buenos Aires

Congreso; II Congreso Argentino de Microscopía; 2012

Asociación Argentina de Microscopía (SAMIC)

Brain damage resulting from a combination of hypoxia and reduced cerebral blood flow (ischemia) in the fetus and newborn infant remains a major cause of death and disability in children, being cerebral palsy, mental retardation, and epilepsy among the most common complications [1][2][3][4]. The incidence of severe perinatal asphyxia is estimated of about 1/1000 live births in developed countries, having an incidence of 5 to 10/1000 live births in developing countries [5]. The production of reactive oxygen species (ROS) has been proposed as an important cause of neuronal death and consequently brain damage after ischemia reperfusion [6]. Currently, several therapeutic approaches for the destruction of oxygen free radicals generated during and following hypoxia ischemia have been proposed. Such as the administration of specific enzymes known to degrade highly reactive radicals to a non reactive component, free radical inhibitors, and scavengers [5]. At present, no individual neuroprotective agents have been proven safe and effective for the protection of neonates from neurological sequels after a hypoxic ischemic insult. The insight into the biochemical and cellular mechanisms of neuronal injury with perinatal hypoxia ischemia helps to provide interventions to interrupt those deleterious cascades, principally focusing on the potential effects of free radical scavengers [7]. Nowadays, we look at Thioredoxins (Trxs) a crucial protein family for antioxidative defense, the modulation of intra and extracellular signalling pathways, the regulation of transcription factors, and the modulation of immune response, and new functions of Trxs are described almost on a weekly basis [8]. In the present work, we study the differential expression of the oxidoreductases of the Trxs of proteins, and their role in the cellular response to oxidative stress in a modified model of perinatal hypoxic ischemia developed by Rice (1981) [1] and Levine (1960) [9]. At a molecular level we have observed several remarkable differences in both abundance and regional distribution of Trxs (this family) of proteins at different times. Combining Western Blot and light microscopy analysis, we have observed some remarkable differential expression of these proteins in the most vulnerable areas of the brain to hypoxia ischemia.