Effect of miR-506-3p on Proliferation and Apoptosis of Airway Smooth Muscle Cells in Asthmatic Mice by Regulating CCL2 Gene Expression and Mediating TLR4/NF-κB Signaling Pathway Activation.

We aimed to investigate the effect of miR-506-3p on the proliferation and apoptosis of airway smooth muscle cells (ASMCS) in asthmatic mice by regulating the activation of TLR4/NF-κB signaling pathway through targeted regulation of C-C Motif Chemokine Ligand 2 (CCL2) expression. Twenty-four BALB/c mice of specific pathogen-free grade were selected to establish asthmatic mouse model, which were randomly divided into normal control group and asthma model group (n = 12 for each group). HE and IHC staining, bioinformatics and dual luciferase reporter assay, RT-PCR MTT, flow cytometry and Western blot were used in this research. HE staining showed airway epithelium thickening, submucosal inflammatory cell infiltration and airway smooth muscle thickening, and the positive expression rate of CCL2 was significantly increased in asthma model group (all P   0.05). Overexpression of miR-506-3p can inhibit ASMCS proliferation and promote apoptosis via inhibiting CCL2 expression and suppressing the activation of TLR4/NF-κB signaling pathway. Inhibited expression of miR-506-3p can reverse the positive role of CCL2 gene silencing. Our study is the first to prove the beneficial role of miR-506-3p-CCL2-TLR4/NF-κB regulatory axis in the development of asthma.