College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China.
College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China.
Redox Biol. 2021 Aug;44:102003. doi: 10.1016/j.redox.2021.102003. Epub 2021 May 18.
Selenium (Se) deficiency and poor plasma Se levels can cause cardiovascular diseases by decreasing selenoprotein levels. Neutrophil extracellular traps (NETs) may be the vicious cycle center of inflammation in vasculitis. Here, we show that Se deficiency induced arteritis mainly by reducing selenoprotein S (SelS), and promoted the progression of arteritis by regulating the recruitment of neutrophils and NET formation. Silencing SelS induced chicken arterial endothelial cells (PAECs) to secrete cytokines, and activated neutrophils to promote NET formation. Conversely, scavenging DNA-NETs promoted cytokine secretion in PAECs. The NET formation regulated by siSelS was dependent on a reactive oxygen species (ROS) burst. We also found that the PPAR pathway was a major mediator of NET formation induced by Se-deficient arteritis. Overall, our results reveal how Se deficiency regulates NET formation in the progression of arteritis and support silencing-SelS worsens arteritis.
硒（Se）缺乏和血浆硒水平低下可通过降低硒蛋白水平导致心血管疾病。中性粒细胞胞外诱捕网（NETs）可能是血管炎中炎症的恶性循环中心。在这里，我们表明，硒缺乏主要通过减少硒蛋白 S（SelS）诱导动脉炎，并通过调节中性粒细胞募集和 NET 形成促进动脉炎的进展。沉默 SelS 诱导鸡动脉内皮细胞（PAECs）分泌细胞因子，并激活中性粒细胞促进 NET 形成。相反，清除 DNA-NETs 促进 PAECs 中细胞因子的分泌。siSelS 调节的 NET 形成依赖于活性氧（ROS）爆发。我们还发现，PPAR 途径是硒缺乏性动脉炎诱导的 NET 形成的主要介质。总的来说，我们的结果揭示了硒缺乏如何调节动脉炎进展中的 NET 形成，并支持沉默 SelS 会加重动脉炎。
