Downregulation of miR‑409‑3p suppresses LPS‑induced inflammation in human bronchial epithelial cells through SOCS3/JAK1/STAT3 signaling: The implication for bronchopneumonia
Affiliations: Department of Pediatrics, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, P.R. China
- Published online on: January 6, 2021 https://doi.org/10.3892/mmr.2021.11829
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
In recent decades, the role of microRNAs (miRs) in the development of pneumonia has been reported by a number of researchers. The present study aimed to investigate the role of miR‑409‑3p in lipopolysaccharide (LPS)‑induced human bronchial epithelial cells and the implication for bronchopneumonia. An in vitro inflammation model was established using LPS‑induced BEAS‑2B cells. Cell apoptosis was determined by flow cytometry. Inflammatory factors were detected by ELISA and reverse transcription‑quantitative PCR. Protein levels of Janus kinase 1 (JAK1)/STAT3 and suppressor of cytokine signaling (SOCS)3 were determined by western blotting. Dual‑luciferase reporter assay was performed to confirm the interaction between miR‑409‑3p and SOCS3. LPS treatment significantly increased miR‑409‑3p expression and decreased the expression levels of SOCS3 in BEAS‑2B cells. Dual‑luciferase reporter assay demonstrated that miR‑409‑3p directly targeted and negatively regulated SOCS3. Inhibition of miR‑409‑3p markedly decreased the levels of TNF‑α, IL‑6 and IL‑1β, and suppressed apoptosis induced by LPS, which was reversed by SOCS3‑knockdown. The inhibition of SOCS3 significantly activated JAK1/STAT3 signaling, as well as enhancing the levels of TNF‑α, IL‑6 and IL‑1β, and promoting apoptosis, which was reversed by the JAK1 inhibitor Tofacitinib. Suppression of miR‑409‑3p improved LPS‑induced inflammation through SOCS3 in LPS‑treated BEAS‑2B cells, and this may be caused by regulating JAK1/STAT3 signaling.