miR-3934 suppresses basophil apoptosis and secretion of inflammatory cytokines by targeting RAGE in asthma

Abstract

Background Several miRNAs are now known to have clear connections to the pathogenesis of asthma. The present study focused on the potential role of miR-3934 during asthma development. Methods The basophils was isolated from 50 asthmatic patients and 50 health controls. The expression level of miR-3934 was examined by RT-qPCR and the expression of receptor for advanced glycation end products (RAGE) was detected by western blot. In addition, the analysis of apoptotic basophils was performed by flow cytometry; the expression level of inflammatory cytokines was detected by ELISA kits; and several important proteins in TGF-β/Smad signaling were examined by western blot. Results miR-3934 was down-regulated in the basophils of asthmatic patients. The expression of the pro-inflammatory cytokines IL-6, IL-8 and IL-33 was enhanced in basophils from asthmatic patients, and this effect was partially reversed by transfection of miR-3934 mimics. Furthermore, receiver operating characteristics analysis showed that miR-3934 levels can be used to distinguish asthma patients from healthy individuals. miR-3934 partially inhibited advanced glycation end products-induced increases in basophil apoptosis by suppressing expression of RAGE. Conclusion Our results indicate that miR-3934 acts to mitigate the pathogenesis of asthma by targeting RAGE and suppressing TGF-β/Smad signaling.