TRAF3 promoted ROS-induced oxidative stress in model of cardiac infarction through the regulation of ULK1 ubiquitination.

Abstract

Obejectives: Cardiac infarction is a dynamic, nonlinear and unpredictable course of disease, and who die of acute myocardial infarction, and coronary thrombosis. TRAF3 provide novel targets for the clinical prevention and treatment for tumors, viral infection, and so on.We investigated the mechanisms of TRAF3 gene, which plays a possible role in cardiac infarction and contributes to the pathogenesis of cardiac infarction-induced oxidative stress.

Methods: Serum samples of patients with cardiac infarction and normal healthy volunteers were obtained from the 920 Hospital of PLA joint service support force. C57BL/6 mice were ligated and H9C2 cells were induced with 1% O2,5%CO2 and 94% N2.

Results: The mRNA expression levels of TRAF3 in patients with cardiac infarction were increased, compared to healthy volunteers. Serum mRNA of TRAF3 was in positive correlation with serum CK levels in patients with cardiac infarction. Over-expression of TRAF3 heightened ROS-induced oxidative stress in vitro model of cardiac infarction. Then, TRAF3 recombinant protein could promote oxidative stress and aggravated cardiac infarction in mice model. Over-expression of TRAF3 induced ULK1 protein expression and reduced ULK1 ubiquitination in vitro model. The activation of ULK1 reduced the effects of TRAF3 on oxidative stress in vitro model of cardiac infarction. Meanwhile, the inhibition of ULK1 reversed the effects of si-TRAF3 on oxidative stress in vitro model of cardiac infarction.

Conclusions: This study identified that TRAF3 promoted ROS-induced oxidative stress in model of cardiac infarction through the regulation of ULK1 ubiquitination, which could potentially give rise to a new strategy for the treatment of cardiac infarction.