MiR-323b-5p regulates the development of childhood asthma by targeting the RNF24 gene

Abstract

Childhood asthma is a chronic respiratory disease characterized by airway hyperresponsiveness and chronic inflammation, which involves immune dysregulation and may be associated with microRNA (miRNA) dysregulation. Exploring the clinical significance of miR-323b-5p in childhood asthma, as well as its role and regulatory mechanisms in the pathogenesis of the disease. This study enrolled 76 pediatric asthma patients and 73 healthy controls. Serum and airway smooth muscle cell (hASMC) samples were assessed for miR-323b-5p, RNF24, and α-SMA expression (RT-qPCR) and cytokine levels (ELISA). Pearson correlation and logistic regression were used for analysis, while cell proliferation and migration were evaluated via CCK-8 and Transwell assays. MiR-323b-5p was significantly upregulated in pediatric asthma patients and in PDGF-BB-induced human airway smooth muscle cells (hASMCs), whereas its putative target, RNF24, was downregulated. Clinically, elevated miR-323b-5p levels demonstrated strong diagnostic potential and served as an independent risk factor for childhood asthma. Functionally, miR-323b-5p inhibition mitigated PDGF-BB-induced hASMC proliferation, migration, and inflammatory response. Critically, these suppressive effects were reversed upon co-knockdown of RNF24, confirming that miR-323b-5p functions by directly targeting RNF24. MiR-323b-5p demonstrates diagnostic potential in childhood asthma by promoting disease progression through targeting RNF24, suggesting its promise as a therapeutic target.