Gene

Myeloperoxidase

Cell biology

Biology

Selenoprotein P

Reactive oxygen species

Cancer research

Biochemistry

Gene silencing

Secretion

Glutathione peroxidase

Immunology

Superoxide dismutase

NADPH oxidase

Oxidative stress

Inflammation

Selenium deficiency

Internal medicine

Arteritis

Medicine

Chemistry

Neutrophil extracellular traps

Selenoprotein

Redox Biology

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.

Roles of selenoprotein S in reactive oxygen species-dependent neutrophil extracellular trap formation induced by selenium-deficient arteritis