Abstract As a chronic airway disease, asthma has two characteristics, tissue remodeling and airway inflammation. This research focused on miR-92a to explore how it works in asthma. We revealed that the expressions of miR-92a were decreased in both serum and lung tissues from ovalbumin-induced asthma mouse. Bioinformatics analysis, quantitative polymerase chain reaction (qPCR) and dual luciferase assay revealed that miR-92a targets MUC5AC, which was linked to mucus hypersecretion in the pulmonary tracts. By injecting miR-92a-mimics into the trachea, both the airway hyper-reactivity and airway inflammation can be alleviated in an asthma mouse model which is induced by ovalbumin. Moreover, the goblet cell phenotype of asthmatic mice is significantly reduced by the action of miR-92a. Furthermore, miR-92a blocked interleukin (IL)-13-induced MUC5AC luciferase activity in 16HBE. Together, upregulation of miR-92a expression in asthmatic mice plays a role in blocking goblet cell metaplasia by targeting MUC5AC, and thus in the treatment of chronic airway diseases, miR-92a can prevent epithelial remodeling, which is a reasonable method.

中文翻译：

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miR-92a的上调通过靶向哮喘中的MUC5AC来阻断杯状细胞化生

摘要 作为一种慢性气道疾病，哮喘具有组织重塑和气道炎症两个特征。这项研究的重点是 miR-92a，以探索它在哮喘中的作用。我们发现，来自卵清蛋白诱导的哮喘小鼠的血清和肺组织中 miR-92a 的表达均降低。生物信息学分析、定量聚合酶链反应 (qPCR) 和双荧光素酶测定显示 miR-92a 靶向 MUC5AC，这与肺道中的粘液分泌过多有关。通过将 miR-92a 模拟物注射到气管中，在由卵清蛋白诱导的哮喘小鼠模型中，气道高反应性和气道炎症都可以得到缓解。此外，miR-92a 的作用显着降低了哮喘小鼠的杯状细胞表型。此外，miR-92a 在 16HBE 中阻断白细胞介素 (IL)-13 诱导的 MUC5AC 荧光素酶活性。总之，在哮喘小鼠中上调 miR-92a 表达通过靶向 MUC5AC 来阻断杯状细胞化生，因此在慢性气道疾病的治疗中，miR-92a 可以防止上皮重塑，这是一种合理的方法。