info:eu-repo/semantics/article
Cardiac ischemic preconditioning prevents dystrophin proteolysis by MMP-2 inhibition
Fecha
2016-09Registro en:
Rodríguez, Manuel; Buchholz, Bruno; D'Anunzio, Verónica; Donato, Martin; González, Germán Esteban; et al.; Cardiac ischemic preconditioning prevents dystrophin proteolysis by MMP-2 inhibition; Instituto de Histología y Embriología; Biocell; 40; 1; 9-2016; 43-46
0327-9545
0327-9545
CONICET Digital
CONICET
Autor
Rodríguez, Manuel
Buchholz, Bruno
D'Anunzio, Verónica
Donato, Martin
González, Germán Esteban
Goyeneche, Maria Ailin
Mazo, Tamara Magali
Pérez, Virginia
Wilensky, Luciana
Gelpi, Ricardo Jorge
Resumen
Dystrophin is a membrane-associated protein responsible for structural stability of the sarcolemma in cardiac myocytes and is very sensitive to ischemic damage. The goal of our study was to determine if ischemic preconditioning could prevent dystrophin breakdown through inhibition of matrix metalloproteinase-2 (MMP-2) activity. Isolated rabbit hearts were subjected to global ischemia with or without reperfusion in order to evaluate if dystrophin is preserved by ischemic preconditioning through MMP-2 inhibition. Ischemic preconditioning significantly reduced the infarct size induced by 30 min of ischemia and 180 min of reperfusion. Importantly, it also diminished dystrophin proteolysis and attenuated MMP-2 activity after 30 min ischemia. Thus, our study shows a novel protective role of ischemic preconditioning as a mechanism of preservation of plasma membrane integrity by inhibiting MMP-2 activation.