Thioredoxin-1 attenuates ventricular and mitochondrial post-ischemic dysfunction in the stunned myocardium of transgenic mice

PEREZ V; DANNUNZIO V; VALDEZ LB; ZAOBORNYJ T; BOMBICINO S; MAZO T; LONGO CARBAJOSA N; GIRONACCI M; BOVERIS A; SADOSHIMA J; GELPI RJ

ANTIOXIDANTS & REDOX SIGNALING

MARY ANN LIEBERT INC

Lugar: New York; Año: 2016 vol. 25 p. 78 - 88

1523-0864

Aim: We evaluated the effect of Trx1 system on post-ischemic ventricular and mitochondrial dysfunction using transgenic mice overexpressing cardiac Trx1 and a dominant negative (DN-Trx1) mutant (C32S/C35S) of Trx1. Langendorff-perfused hearts were subjected to 15 min of ischemia followed by 30 min of reperfusion (R). We measured left ventricular developed pressure (LVDP, mmHg), end diastolic pressure (LVEDP, mmHg) and t63 (relaxation index, msec). Mitochondrial respiration, SERCA2a, phospholamban (PLB), and p-PLB Thr 17 expression (Western blot) were also evaluated. Results: At 30 min of reperfusion Trx1 improved contractile state (LVDP: Trx1: 57.4±4.9 vs. Wt: 27.1±6.3 and DN-Trx1: 29.2±7.1, p