Dysfunction of thioredoxin triggers inflammation through activation of autophagy in chicken cardiomyocytes
Dysfunction of thioredoxin triggers inflammation through activation of autophagy in chicken cardiomyocytes
复制标题
硫氧还蛋白功能障碍通过激活鸡心肌细胞自噬引发炎症
作者：
Yang Jie;Gong Yafan;Cai Jingzeng;Liu Qi;Zhang Yuan;Zheng Yingying;Yu Dahai;Zhang Ziwei
硫氧还蛋白（Txn）是一种广泛存在于生物体中的载氢蛋白。Txn缺乏与心肌细胞损伤有关已被证实。然而，确切的机制尚不清楚。为了了解Txn抑制后心肌细胞的反应机制，我们采用基因干扰技术（siRNA）和Txn抑制剂（PX‐12）在心肌细胞中建立了Txn功能障碍模型。我们检测了ROS水平、炎症因子和自噬和凋亡的关键蛋白。此外，还利用热图进行进一步分析。我们的研究结果表明，Txn功能障碍通过上调Becline‐1，LC3‐1,2来增加ROS的释放，诱导自噬的激活，从而进一步调节炎症反应，同时，Txn沉默通过抑制Caspase‐3来抑制鸡心肌细胞的凋亡。总之，我们得出结论，Txn缺失的鸡心肌细胞发生自噬，引起严重的炎症反应并导致心肌细胞损伤。
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.