Michelle Caroline;Timothy Michelsen; David M. Lorenz; Kathrin A.Dorfmüller
Abstract
Inflammasomes are a group of protein complexes built around several proteins, including NLRP3, NLRC4, AIM2 and NLRP6. Recognition of a diverse range of microbial, stress and damage signals by inflammasomes results in direct activation of caspase-1, which subsequently induces secretion of potent pro-inflammatory cytokines and a form of cell death called pyroptosis. In the process of cardiac transplantation, the heart flushed and stored in cold preservation solution and then subsequently re-implanted and reperfused with warm blood. Its also occurs in several important clinical contexts including percutaneous coronary interventions for acute myocardial ischemia, and cardiac surgery in the setting of cardiopulmonary bypass. We performed heterotopic cardiac transplants in both wild-type mice and mice deficient in AIM 2 signaling due to a point mutation. Our data revealed that mice deficient in AIM 2 has evidenced of protction against cold I/R by improved cardiac function, inflammasomes/NLRP3, Bcl-2, Akt phosphorylation, and reduced myocardial apoptosis, Bax expression.
Keywords: Global myocardial I/R; AIM 2;Inflammasomes; NLRP3
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