Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

Abstract

Background Pneumonia is a common acute lower respiratory infection in children and elders. Circular RNAs (circRNAs) have recently been uncovered to play important roles in pneumonia. However, the function and mechanism of circ_0038467 in pneumonia remain elusive. Methods Cell viability and apoptosis were determined using the Cell Counting Kit‐8 (CCK‐8) assay and flow cytometry, respectively. The levels of interleukin 6 (IL‐6), IL‐8 and IL‐1β were detected by enzyme‐linked immunosorbent assay (ELISA). Western blot analysis was performed to assess the expression of related proteins. Circ_0038467 was characterized by Ribonuclease R (RNase) digestion and subcellular localization assays. The levels of circ_0038467 and miR‐338‐3p were evaluated by quantitative real‐time polymerase chain reaction (qRT‐PCR). The direct interaction between circ_0038467 and miR‐338‐3p was validated by the dual‐luciferase reporter and RNA immunoprecipitation (RIP) assays. Results Our data indicated that lipopolysaccharide (LPS) induced an inflammatory injury in 16HBE cells by repressing cell viability and enhancing cell apoptosis and proinflammatory cytokines production. Circ_0038467 was upregulated and miR‐338‐3p was downregulated in LPS‐treated 16HBE cells. Circ_0038467 knockdown or miR‐338‐3p overexpression attenuated LPS‐induced 16HBE cell inflammatory injury. Moreover, circ_0038467 acted as a sponge of miR‐338‐3p in 16HBE cells. MiR‐338‐3p mediated the alleviated effect of circ_0038467 knockdown on LPS‐induced 16HBE cell inflammatory injury. Additionally, the Janus kinase/ signal transducer and activator of transcription 3 (JAK/STAT3) signaling pathway was involved in the circ_0038467/miR‐338‐3p axis‐mediated regulation in LPS‐induced 16HBE cell inflammatory injury. Conclusions The current work had led to the identification of circ_0038467 knockdown that alleviated LPS‐induced inflammatory injury in 16HBE cells at least partly through sponging miR‐338‐3p and regulating JAK/STAT3 pathway, highlighting novel molecular targets for the treatment of pneumonia.

Keywords

• 16HBE cells
• circ_0038467
• inflammatory injury
• miR‐338‐3p
• pneumonia