Dysfunction of thioredoxin triggers inflammation through activation of autophagy in chicken cardiomyocytes.

Abstract

Thioredoxin (Txn) is a hydrogen carrier protein and exists widely in organism. Txn deficiency implicates cardiomyocytes injury has been proven. However, the exact mechanism remains unclear. To understand the mechanistic response of cardiomyocytes subsequent to Txn suppression, we established the model of Txn dysfunction by employing gene interference technology (siRNA) and Txn inhibitor (PX-12) in cardiomyocytes. We detected the ROS levels, inflammation factors, and key proteins in the autophagy and apoptosis. In addition, heat map was used for further analysis. Our results revealed that Txn dysfunction increased the release of ROS and induced activation of autophagy via upregulation of Becline-1, LC3-1, 2, which further regulated the inflammatory response, meanwhile, Txn silence inhibited apoptosis in chicken cardiomyocytes through Caspase-3 inhibition. Altogether we concluded that Txn-deficient chicken cardiomyocytes experienced autophagy, which caused severe inflammatory reactions and resulting in damage to cardiomyocytes.