miR-30a-3p participates in the development of asthma by targeting CCR3

• Main Authors: Li Xiaobo, Wang Binliang, Huang Mao, Wang Xiaomi
• Format: Article
• Language: English
• Published: De Gruyter 2020-06-01
• Series: Open Medicine
• Subjects: mir-30a-3p; ccr3; ovalbumin; asthma; eosinophils
• Online Access: https://doi.org/10.1515/med-2020-0102

This study aimed to investigate the role and relevant mechanism of miR-30a-3p action in asthma. The results of this study revealed that the expression levels of miR-30a-3p were significantly decreased in the peripheral blood of asthmatic patients. In addition, we found that the CC chemokine receptor (CCR3) was a target of miR-30a-3p. Subsequently, an asthma mouse model was established using ovalbumin (OVA). The results showed that the expression of miR-30a-3p and CCR3 was downregulated and upregulated, respectively, in the peripheral blood of asthmatic mice. Enzyme-linked immunosorbent assay (ELISA) in asthmatic mouse serum demonstrated that miR-30a-3p mimic treatment significantly decreased the secretion of OVA-specific IgE, eotaxin-1, interleukin (IL)-5, and IL-4. These results suggested that miR-30a-3p inhibited CCR3 signaling pathway and relieved the inflammatory response against asthma in vivo. Eosinophils have also been implicated in the asthmatic inflammatory response. Therefore, the in vitro effects of miR-30a-3p on eosinophil activity were determined. Findings suggested that miR-30a-3p mimic significantly reduced eosinophil viability and migration and induced apoptosis. In addition, CCR3 and eotaxin-1 downregulation were observed. The aforementioned results were significantly reversed following CCR3 overexpression. This study suggested that miR-30a-3p was involved in asthma by regulating eosinophil activity and targeting CCR3.