Long non-coding RNA00882 contributes to platelet-derived growth factor-induced proliferation of human fetal airway smooth muscle cells by enhancing Wnt/β-catenin signaling via sponging miR-3619-5p.

Long non-coding RNAs (lncRNAs) are emerging as novel and critical regulators in the pathogenesis of asthma. However, the precise role of lncRNAs in pediatric asthma remains largely unknown. In this study, we aimed to investigate the biological function of lncRNA00882 (LINC00882) in regulating the proliferation of fetal airway smooth muscle (ASM) cells, which play an important role in airway remodeling during asthma development. Herein, we found that LINC00882 expression was significantly up-regulated in ASM cells stimulated with platelet-derived growth factor (PDGF). Functional experiments showed that the knockdown of LINC00882 markedly reduced the proliferation of fetal ASM cells induced by PDGF, while the overexpression of LINC00882 exhibited the opposite effect. Bioinformatics analysis, the luciferase reporter assay and the RNA pull-down assay revealed that LINC00882 directly interacted with microRNA-3619-5p (miR-3619-5p). LINC00882 negatively regulated miR-3619-5p expression in fetal ASM cells. Notably, β-catenin was identified as a target gene of miR-3619-5p. miR-3619-5p overexpression restricted PDGF-induced cell proliferation through inhibiting Wnt/β-catenin signaling. Moreover, miR-3619-5p overexpression significantly attenuated the LINC00882-induced promotion effect on PDGF-induced cell proliferation and Wnt/β-catenin signaling in fetal ASM cells. In contrast, miR-3619-5p inhibition significantly reversed the LINC00882 knockdown-mediated inhibitory effect on PDGF-induced cell proliferation and Wnt/β-catenin signaling. Taken together, our results demonstrate that LINC00882 promotes PDGF-induced cell proliferation of ASM cells by enhancing Wnt/β-catenin signaling via sponging miR-3619-5p, suggesting a potential role for LINC00882 in airway remodeling in pediatric asthma.

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