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Artículo

Inhibition of endogenous thioredoxin-1 in the heart of transgenic mice does not confer cardioprotection in ischemic postconditioning

Perez, María VirginiaIcon ; D'Anunzio, VerónicaIcon ; Mazo, Tamara MagaliIcon ; Marchini, Timoteo OscarIcon ; Caceres, Lourdes Catalina; Evelson, Pablo AndrésIcon ; Gelpi, Ricardo JorgeIcon
Fecha de publicación: 12/2016
Editorial: Pergamon-Elsevier Science Ltd
Revista: International Journal of Biochemistry and Cellular Biology
ISSN: 1357-2725
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Fisiología

Resumen

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<0.05), but this protection was abolished in DN-Trx1-PostC group (49.7±1.1%). The ischemia/reperfusion and postconditioning in mice overexpressing thioredoxin-1 reduced infarct size at the same magnitude (35.9±2.1 and 38.4±1.3%, p<0.05 vs. Wt-I/R). In Wt-PostC, Trx1-I/R and Trx1- PostC, Akt and GSK3β phosphorylation increased compared to Wt-I/R, without changes in DN-Trx1 groups. In conclusion, given that the cardioprotection conferred by thioredoxin-1 overexpression and postconditioning, is accomplished through the activation of the Akt/GSK3β survival pathway, no synergic effect was evidenced. Thioredoxin-1 plays a key role in the postconditioning, given that when this protein is inactive the cardioprotective mechanism was abolished. Thus, diverse comorbidities or situations modifying the thioredoxin activity, could explain the absence of this strong mechanism of protection in different clinical situations.
Palabras clave: Dominant Negative of Trx1 , Ischemic Postconditioning , Myocardial Infarction , Oxidative Stress , Thioredoxin-1
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info:eu-repo/semantics/restrictedAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
Identificadores
URI: http://hdl.handle.net/11336/47651
DOI: https://dx.doi.org/10.1016/j.biocel.2016.09.017
URL: https://www.sciencedirect.com/science/article/pii/S1357272516302795
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Articulos(IBIMOL) [398]
Articulos de INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR
Citación
Perez, María Virginia; D'Anunzio, Verónica; Mazo, Tamara Magali; Marchini, Timoteo Oscar; Caceres, Lourdes Catalina; et al.; Inhibition of endogenous thioredoxin-1 in the heart of transgenic mice does not confer cardioprotection in ischemic postconditioning; Pergamon-Elsevier Science Ltd; International Journal of Biochemistry and Cellular Biology; 81; 12-2016; 315-322
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