Abstract
ObjectiveTo characterize microRNA-206 (miR-206) in the development of bronchopulmonary dysplasia (BPD).Design/MethodsWe assessed the expression of miR-206 in BPD mouse lung tissues and blood samples of BPD patients by quantitative real-time PCR. Then, the role of miR-206 in regulating cell biology were examined by XTT assay, flow cytometry, transwell invasion assay, wound healing assay and adhesion assay in vitro. Furthermore, luciferase reporter assay, real-time PCR, western blot and Immunofluorescence staining were performed to figure out the target gene of miR-206.ResultsA reduction in expression of miR-206 was observed in BPD mice compared with controls and in BPD patients compared with controls. miR-206 overexpression significantly induced cell apoptosis, reduced cell proliferation, migration and adhesion abilities, whereas the inhibition of miR-206 expression had the opposite effect. Fibronectin 1 (FN1) is a direct target of miR-206, and fn 1 can be transcriptionally and translationally regulated by miR-206. Down-regulation of miR-206 modulates biological functions of the cells, at least in part, by increasing the level of fn 1. Furthermore, fn 1 expression levels were increased in the BPD mice and BPD patients.ConclusionsThe expression of miR-206 and its target gene, fn 1, may contribute to the progression of BPD.
Highlights
Babies born prematurely or who experience respiratory problems shortly after birth are at risk for bronchopulmonary dysplasia (BPD), which is a common chronic lung disease with a multifactorial etiology that manifests in preterm neonates
We report here that miR-206 is down-regulated in BPD patients and BPD newborn mice, and miR-206 targets fibronectin 1 (FN1), an extracellular matrix (ECM) glycoprotein that is involved in cell adhesion and migration processes including embryogenesis, wound healing, metastasis, and host defense [7]
Among these miRNAs, we found in this study that BPD mice had decreased expression of miR-206 compared to the air-exposed control mice
Summary
Babies born prematurely or who experience respiratory problems shortly after birth are at risk for bronchopulmonary dysplasia (BPD), which is a common chronic lung disease with a multifactorial etiology that manifests in preterm neonates. Up to 70% of babies born before 26 weeks of gestation develop BPD [1,2]. Several lines of evidence indicate that a severely perturbed extracellular matrix (ECM) metabolism contributes to this disorder [3], the underlying pathogenesis is not fully understood, and no evidence-based strategies to prevent or treat BPD are currently available. We previously demonstrated that miRNAs are associated with lung development and that altered miRNA levels contribute to the development of BPD [5,6]. We report here that miR-206 is down-regulated in BPD patients and BPD newborn mice, and miR-206 targets fibronectin 1 (FN1), an ECM glycoprotein that is involved in cell adhesion and migration processes including embryogenesis, wound healing, metastasis, and host defense [7]. Our results may reflect an important role for miR-206-mediated ECM remodeling during the development of BPD
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