| First Author | Fang C | Year | 2016 |
| Journal | PLoS One | Volume | 11 |
| Issue | 3 | Pages | e0149257 |
| PubMed ID | 26959414 | Mgi Jnum | J:249012 |
| Mgi Id | MGI:6092935 | Doi | 10.1371/journal.pone.0149257 |
| Citation | Fang C, et al. (2016) MiR-3162-3p Is a Novel MicroRNA That Exacerbates Asthma by Regulating beta-Catenin. PLoS One 11(3):e0149257 |
| abstractText | Asthma is a common chronic respiratory disease. In a previous study, we found several circulating microRNA signatures associated with childhood asthma and selected miR-3162-3p for subsequent studies. Since the target proteins and underlying molecular mechanisms of miR-3162-3p in asthma etiopathogenesis are not well characterized, we designed this study to clarify its role. We employed bioinformatics and quantitative PCR methods as a first step to determine the target of miR-3162-3p, and we elucidated beta-catenin. Luciferase assays and western blot analysis confirmed beta-catenin as a direct target of miR-3162-3p as the 3'-untranslated region of beta-catenin mRNA possesses a specific miR-3162-3p pairing site. The correlation between the expression levels of miR-3162-3p and beta-catenin is confirmed by quantitative PCR and western blot studies in A549, Beas-2B and H1299 cell lines and OVA-induced asthma mouse model. Of note, upregulation of the endogenous miR-3162-3p level is concomitant with the reduction of beta-catenin mRNA and protein expression levels. MiR-3162-3p antagomir treatment antagonizes the endogenous miR-3162-3p and effectively rescues the attenuation of endogenous beta-catenin in OVA-induced asthmatic mice, which alleviates airway hyperresponsiveness and ameliorates airway inflammation. Collectively, our findings suggest a novel relationship between miR-3162-3p and beta-catenin and clarify their mechanistic role in asthma etiopathogenesis. |
