MicroRNA ‑17 contributes to the suppression of the inflammatory response in lipopolysaccharide‑induced acute lung injury in mice via targeting the toll‑like receptor 4/nuclear factor‑κB pathway.

MicroRNA‑17 contributes to the suppression of the inflammatory response in lipopolysaccharide‑induced acute lung injury in mice via targeting the toll‑like receptor 4/nuclear factor‑κB pathway.
Int J Mol Med. 2020 Jul;46(1):131-140
Authors: Fu S
Abstract
Acute lung injury (ALI) is a common lung disease with a high mortality rate, which is characterized by an excessive uncontrolled inflammatory response. MicroRNA (miR)‑17 has previously emerged as a novel regulatory molecule of inflammatory response in various complex diseases; however, the anti‑inflammatory action and associated molecular mechanisms of miR‑17 in ALI have not been fully elucidated. The aim of the present study was to investigate the role of miR‑17 in the inflammatory response in ALI and to elucidate the potential underlying mechanism. Using a lipopolysaccharide (LPS)‑induced ALI mouse model, it was observed that miR‑17 was significantly downregulated in lung tissues compared with the control group. In this model, ectopic expression of miR‑17 attenuated lung pathological damage, reduced lung wet/dry ratio and lung permeability, and increased survival rate in ALI mice. In addition, agomiR‑17 injection significantly suppressed LPS‑induced inflammation, as evidenced by a reduction in the activity of myeloperoxidase and the production of interleukin (IL)‑6, IL‑1β and tumor necrosis factor‑α in lung tissues. Of note, toll‑like receptor (...

Source: International Journal of Molecular Medicine - June 30, 2020 Category: Molecular Biology Authors: Fu S Tags: Int J Mol Med Source Type: research