154 - Expression of Redox Proteins in the Heart After Myocardial Infarction in Rats

Abstract

Ischemic diseases, among others, myocardial infarction (MI), are the leading causes of death worldwide. MI is associated with a high tissue damage due in part to the activation of the immune response and the generation of reactive oxygen species (ROS), both taking place mainly during the reperfusion phase, once the blood supply to the tissue is restored. In spite of the harmful effects of ischemia and reperfusion, some injured cells manage to survive by activating endogenous defense mechanisms. Thioredoxins (Trxs) and peroxiredoxins (Prxs) are recognized as key molecules in redox signaling, regulating oxidative post-translational modifications of proteins (Trxs) and cellular levels of hydrogen peroxide (Prxs). Based on the strong evidence for a role of interrupted redox signaling in ischemia-reperfusion pathologies, we believe that Trxs and Prxs are potential defense mechanisms upregulated during ischemia-reperfusion damage. Using immunohistochemistry and Western blot analysis, we investigated the expression pattern of Trx1, Trx reductase 1, Trx2, Prx1, and Prx2 in the heart of rats one week after MI or sham operation. Trx1, Prx1, and Prx2 were upregulated in the heart after MI. Trx1 showed the strongest immunostainings after MI and was detected not only in cardiomyocytes, but also in various immune cell populations infiltrating the infarcted area. Interestingly, Trx1 changed its classical cytosolic localization observed in sham operated animals and was translocated into the cell nucleus of cardiomyocytes after MI. Trx1 was also detected in the serum of animals two days after MI. Trx reductase 1 and mitochondrial Trx2 did not show any changes after MI. These findings point to a putative role of Trx1 in the defense against IR-induced tissue damage in the heart that may be important, for instance, for cell survival and the modulation of the immune response.