Abstract

Allergic inflammation and airway remodeling frequently occur in asthma. This study clarifies a novel LINC1810064F22Rik-mediated ceRNA mechanism involved in asthma-induced allergic inflammation and airway remodeling based on bioinformatics analysis and in vivo and in vitro experiments. The differentially expressed lncRNAs and downstream effectors were predicted in silico . The targeting relationship among LINC1810064F22Rik, miR-206-5p, and HDAC4 was predicted by bioinformatics analysis, which was further validated by dual luciferase reporter gene assay. The asthma-like airway inflammation was induced in mice using ovalbumin (OVA) sensitization/challenge with immune adjuvant Al(OH) 3 , while alveolar epithelial cells (AECs) were exposed to IL-33 to mimic in vitro inflammatory environment. LINC1810064F22Rik and HDAC4 were highly expressed, while miR-206-5p was poorly expressed in the tracheal tissues of OVA mice and the IL-33-treated AECs. The OVA mice and IL-33-treated AECs were subjected to gain- or loss-of-function experiments to detect the interaction of LINC1810064F22Rik/miR-206-5p/HDAC4 axis and their effects on allergic inflammation and airway remodeling. LINC1810064F22Rik competitively bound to miR-206-5p, and miR-206-5p targeted and inhibited HDAC4. The in vivo animal experiments indicated that LINC1810064F22Rik promoted asthma-induced allergic inflammation and airway remodeling by sequestering miR-206-5p away from HDAC4. The evidence provided by our study highlighted the involvement of the LINC1810064F22Rik/miR-206-5p/HDAC4 axis in facilitating allergic airway inflammation and airway remodeling in OVA mice.