SOCS3 limits TNF and endotoxin-induced endothelial dysfunction by blocking a required autocrine interleukin-6 signal in human endothelial cells

• Published in: American Journal of Physiology: Cell Physiology Vol. 323; no. 2; pp. C556 - C569
• Main Authors: Martino, Nina, Bossardi Ramos, Ramon, Chuy, Dareen, Tomaszek, Lindsay, Adam, Alejandro P
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.08.2022
• Subjects: Animals; Endothelial Cells - metabolism; Endothelium - metabolism; Endotoxins - metabolism; Endotoxins - toxicity; Humans; Interleukin-6 - metabolism; Lipopolysaccharides - toxicity; Mice; NF-kappa B - metabolism; Suppressor of Cytokine Signaling 3 Protein - genetics; Suppressor of Cytokine Signaling 3 Protein - metabolism; Suppressor of Cytokine Signaling Proteins - metabolism; endothelium; inflammation; STAT3; permeability; interleukin; interleukin-6; endotoxin

Increased circulating levels of soluble interleukin (IL)-6 receptor α (sIL-6Rα) are commonly observed during inflammatory responses, allowing for IL-6 signaling in cells that express the ubiquitous receptor subunit gp130 but not IL-6Rα, such as endothelial cells. Activation of Toll-like receptor (TL...