MicroRNA-885-3p alleviates bronchial epithelial cell injury induced by lipopolysaccharide via toll-like receptor 4. Issue 3 (1st March 2022)

• Record Type: Journal Article
• Authors: Shen, Yahui; Jiang, Aigui; Chen, Rong; Gao, Xiaoyan; Song, Guixian; Lu, Huiyu
• Is Part Of: Bioengineered. Volume 13:Issue 3(2022)
• Page Start: 5305
• Page End: 5317
• Publication Date: 2022-03-01
• Subjects: Asthma -- MiR-885-3p -- TLR4 -- cell injury -- NF-κB-MyD88 pathway; Biomedical engineering -- Periodicals; Biotechnology -- Periodicals; Microbiology -- Periodicals; 660.6
• DOI: 10.1080/21655979.2022.2032939
• Languages: English
• ISSNs: 2165-5987

Abstract

ABSTRACT: Airway inflammation is one of the typical pathological characteristics of asthma. MicroRNAs (miRNAs) play important roles in regulating inflammation. Nevertheless, miRNA-885-3p (miR-885-3p)'s role in asthmatic inflammation and the underlying mechanism need to be explained. In this work, miR-885-3p expression and toll-like receptor 4 (TLR4) expression in asthma patients' plasma and lipopolysaccharide (LPS)-treated 16HBE cells were detected through quantitative real-time PCR. The interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels in 16HBE cell supernatant were examined via enzyme-linked immunosorbent assay. Cell counting kit-8 (CCK-8) assay and flow cytometry were employed to examine 16HBE cell viability and apoptosis, respectively. Western blotting was performed to examine the expression of TLR4, cleaved caspase-3, B-cell lymphoma-2 (Bcl-2), nuclear factor-kappa B (NF-κB) p65, Bcl-2-related X protein (Bax), phosphorylated (p)-NF-κB p65 and myeloid differentiation primitive-response protein 88 (MyD88) in 16HBE cells. Furthermore, the targeted relationship between TLR4 and miR-885-3p in 16HBE cells was determined through dual-luciferase reporter gene assay. Compared with healthy volunteers, miR-885-3p expression in acute asthma patients' plasma was significantly downregulated. In 16HBE cells, the stimulation of LPS reduced miR-885-3p expression. MiR-885-3p overexpression reduced LPS-stimulated 16HBE cell injury by enhancing cell viability, and suppressing the levels of inflammatory factors and apoptosis. Furthermore, TLR4 was identified as miR-885-3p's target gene. TLR4 overexpression weakened the impacts of miR-885-3p on LPS-stimulated cell injury and NF-κB-MyD88 signaling. In conclusion, miR-885-3p can reduce LPS-induced 16HBE cell damage, via targeting TLR4 to suppress the NF-κB-MyD88 pathway. Graphical abstract: uf0001