期刊
JOURNAL OF INTERNATIONAL MEDICAL RESEARCH
卷 47, 期 7, 页码 3307-3319出版社
SAGE PUBLICATIONS LTD
DOI: 10.1177/0300060518789819
关键词
miR-145-5p; KIF3A; asthma; chemokines; inflammation; epithelial barrier
Background MicroRNA (miR)-145-5p is a respiratory disease biomarker, and is upregulated in asthma pathogenesis. However, its underlying mechanisms were unclear, so were investigated in the present study. Methods A mouse model of asthma was established by challenge with house dust mite (HDM) extract. An miR-145-5p antagomir was administered nasally and expression of kinesin family member 3A (KIF3A) and miR-145-5p was measured by immunohistochemistry, PCR, and western blot. Eosinophils in lavage fluid and levels of interleukin (IL)-4, IL-5, and IL-13 were quantified. Airway hyper-responsiveness was measured and KIF3A expression was tested following miR-145-5p overexpression or interference in the 16HBE14o- airway epithelial cell line. The effects of miR-145-5p and KIF3A co-transfection in 16HBE14o- cells were examined on cytokine release, epithelial barrier dysfunction, and epithelial repair in HDM-exposed cells. Results KIF3A downregulation and miR-145-5p upregulation were noted in airway epithelial cells of HDM-exposed asthmatic mice, while miR-145-5p antagonism significantly improved symptoms. MiR-145-5p promoted the HDM-induced release of chemokines and inflammatory factors and epithelial barrier dysfunction, and suppressed epithelial repair by directly targeting KIF3A. Conclusion miR-145-5p influenced HDM-induced epithelial cytokine release and epithelial barrier dysfunction via regulating KIF3 expression. It also affected epithelial repair, exacerbating the HDM-induced T helper 2-type immune response in mice.
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