The cardioprotection conferred by thioredoxin-1 in ischemic postconditioning is abolished in middle-aged mice.

VIRGINIA PEREZ; VERÓNICA D´ANNUNZIO; TAMARA ZAOBORNYJ; ANABELLA GOMEZ; TAMARA MAZO; VERÓNICA CASANOVA; ELIANA CICALE; RICARDO J. GELPI

CABA

Congreso; Joint meeting of bioscience societies. LXII Annual meeting of argentine society of clinical investigation (SAIC); 2017

Sociedad Argentina de Investigación Clínica

Thioredoxin-1 (Trx1) maintains the cellular redox status and decreasesthe infarct size in ischemia/reperfusion injury (I/R). However,it is not fully understood the role of Trx1 in ischemic postconditioning(PostC) in young and aged mice. The aim was to study if Trx1is involved in the PostC cardioprotection mechanism and if the agecan modify this. Wild type mice hearts (Wt), transgenic mice heartsoverexpressing Trx1, and a dominant negative (DN-Trx1) mutant(C32S/C35S) of Trx1 were used, mice were divided in young group(4 month) and middle-aged group (12 month). The mice hearts weresubjected to 30 min of I and 120 of R (Langendorff technique) (I/Rgroup). In the PostC group, after I, a protocol of 6 cycles of R/I wasperformed. The assessment of the infarct size was performed usingTTC. Also, it was measure hidrogen peroxide (H2O2) production,protein nitration, Trx1 activity and expression and pAkt and pGSK3βexpression (western blot). Data are expressed as mean±SEM andp<0.05 was considered statistically significant. n= 6 each group.Previously, we showed that Trx1 is involved in cardioprotectionconferred by PostC in young mice. Then we performed thesame groups but in middle-aged mice and the cardioprotectionwas abolished in groups with PostC (Wt-PostC: 53.13±4.58%vs Wt-I/R: 51.75±2.64%; DN-Trx1-PostC: 51.17±5.04% vs DNTrx1-I/R: 56.57±4.24% and Trx1-PostC: 51.50±3.94% vs Trx1-I/R:52.88±3.07%). This infarct size behavior was accompanied by a significantlack of survival proteins phosphorylation (Akt and GSK3b)and