1. Inhibition of endogenous thioredoxin-1 in the heart of transgenic mice does not confer cardioprotection in ischemic postconditioning
- Author
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Lourdes Cáceres, Ricardo J. Gelpi, Verónica D´Annunzio, Tamara Mazo, Pablo Evelson, Timoteo Marchini, and Virginia Perez
- Subjects
0301 basic medicine ,Genetically modified mouse ,CIENCIAS MÉDICAS Y DE LA SALUD ,Blotting, Western ,Myocardial Infarction ,Ischemia ,Gene Expression ,Endogeny ,Mice, Transgenic ,Pharmacology ,Fisiología ,medicine.disease_cause ,Biochemistry ,03 medical and health sciences ,Mice ,Thioredoxins ,medicine ,Animals ,Ischemic Postconditioning ,Protein kinase B ,Cardioprotection ,Thioredoxin-1 ,Chemistry ,Myocardium ,Heart ,Cell Biology ,medicine.disease ,Oxidative Stress ,Medicina Básica ,030104 developmental biology ,Phosphorylation ,Dominant Negative of Trx1 ,Reperfusion injury ,Oxidative stress - Abstract
Thioredoxin-1 maintains the cellular redox status and decreases the infarct size in ischemia/reperfusion injury. However, whether the increase of thioredoxin-1 expression or its lack of activity modifies the protection conferred by ischemic postconditioning has not been yet elucidated. The aim was to evaluate if the thioredoxin-1 overexpression enhances the posctconditioning protective effect, and whether the lack of the activity abolishes the reduction of the infarct size. Wild type mice hearts, transgenic mice hearts overexpressing thioredoxin-1, and a dominant negative mutant (C32S/C35S) of thioredoxin-1 were used. The hearts were subjected to 30min of ischemia and 120min of reperfusion (Langendorff) (I/R group) or to postconditioning protocol (PostC group). The infarct size in the Wt-PostC group decreased in comparison to the Wt-I/R group (54.6±2.4 vs. 39.2±2.1%, p
- Published
- 2016