|Public on Dec 27, 2018
|RAW246.1 cells activation by internalized synthetic miR-122
|Expression profiling by array
|Hepatic injury is often accompanied by pulmonary inflammation and tissue damage, but the underneath mechanism is not fully elucidated. Here we identify hepatic miR-122 as a culprit of pulmonary inflammation induced by various liver injuries. Analyses of acute and chronic liver injury mouse models confirm that liver dysfunction can cause pulmonary inflammation and tissue damage. Injured livers release large amounts of miR-122 in a microvesicle-independent manner into the circulation compared to normal livers. Circulating miR-122 is then preferentially transported to mouse lungs and taken up by alveolar macrophages, in which it binds toll-like receptor 7 (TLR7) and activates inflammatory responses. Depleting plasma miR-122 largely abolishes liver injury-induced pulmonary inflammation and tissue damage. Furthermore, alveolar macrophage activation by miR-122 is blocked by mutating the TLR7-binding UG-rich sequence on miR-122 or knocking out macrophage TLR7. Our findings reveal a novel causative role of hepatic miR-122 in liver injury-induced pulmonary dysfunction.
|To explore the molecular basis underlying the effect of hepatic miR-122 on alveolar macrophage inflammatory activation, we performed transcription profiling in macrophages treated with or without miR-122.
|Wang Y, Zen K
|Dec 26, 2018
|Last update date
|Dec 28, 2018
|163 Xianlin Road
|Agilent-026655 Whole Mouse Genome Microarray 4x44K v2 (Probe Name version)