Exportin XPO6 upregulation activates the TLR2/MyD88/NF-κB signaling by facilitating TLR2 mRNA nuclear export in COPD pulmonary monocytes

• Published in: International immunopharmacology Vol. 135; p. 112310
• Main Authors: Wu, Yuting, Gou, Yanni, Wang, Tao, Li, Ping, Li, Yongqiang, Lu, Xing, Li, Weifeng, Liu, Zhifeng
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 30.06.2024
• Subjects: Active Transport, Cell Nucleus; Animals; COPD; Disease Models, Animal; Female; Humans; Karyopherins - metabolism; Lung - immunology; Lung - metabolism; Lung - pathology; Lung inflammation; Male; Mice; Mice, Inbred C57BL; Monocytes - drug effects; Monocytes - immunology; Monocytes - metabolism; Myeloid Differentiation Factor 88 - metabolism; NF-kappa B - metabolism; NF-κB; Pulmonary Disease, Chronic Obstructive - immunology; Pulmonary Disease, Chronic Obstructive - metabolism; Pulmonary monocytes; RNA, Messenger - genetics; RNA, Messenger - metabolism; Signal Transduction; Toll-Like Receptor 2 - genetics; Toll-Like Receptor 2 - metabolism; Toll-like receptors; Up-Regulation; Toll-like receptors; NF-κB; Lung inflammation; Pulmonary monocytes; COPD

•Exportin XPO6 was upregulated in COPD pulmonary monocytes.•XPO6 promoted TLR2 expression in monocytes.•XPO6 enhanced MyD88/NF-κB inflammatory signaling via TLR2.•XPO6 facilitated TLR2 mRNA nuclear export in monocytes. Chronic obstructive pulmonary disease (COPD) poses a significant health threat ch...