{Reference Type}: Journal Article
{Title}: Circ_0035292 knockdown alleviates lipopolysaccharide (LPS)-induced WI-38 cell apoptosis and inflammatory injury.
{Author}: Guo Y;Li Z;Cheng C;
{Journal}: Immun Inflamm Dis
{Volume}: 11
{Issue}: 6
{Year}: 2023 06
{Factor}: 2.493
{DOI}: 10.1002/iid3.905
{Abstract}: Circular RNAs have emerged as important regulators in the pathogenesis of human diseases, including infantile pneumonia (IP). In this study, we aimed to explore the effects of circ_0035292 on lipopolysaccharide (LPS)-treated Wistsar Institute (WI)-38 cells.<BR>Quantitative real-time polymerase chain reaction and western blot were executed to detect the levels of circ_0035292, microRNA-370-3p (miR-370-3p) and transducin β-like 1X related protein 1 (TBL1XR1). Cell counting kit-8, 5-ethynyl-2'-deoxyuridine, and flow cytometry assessed cell proliferation and apoptosis. Concentrations of inflammatory factors were examined with enzyme linked immunosorbent assay kits. Dual-luciferase reporter assay and RNA immunoprecipitation were adopted to analyze binding between miR-370-3p and circ_0035292 or TBL1XR1.<BR>Circ_0035292 level was increased in IP patients and LPS-triggered WI-38 cells. Circ_0035292 knockdown rescued LPS-mediated WI-38 cell proliferation suppression and WI-38 cell apoptosis and inflammation promotion. Circ_0035292 interacted with miR-370-3p and miR-370-3p directly targeted TBL1XR1. Moreover, miR-370-3p overexpression alleviated LPS-induced WI-38 cell apoptosis and inflammatory injury, which was abrogated via TBL1XR1 upregulation. Circ_0035292 absence inhibited the NF-κB pathway.<BR>Knockdown of circ_0035292 rescued LPS-triggered WI-38 cell injury via miR-370-3p/TBL1XR1 axis and NF-κB pathway.