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Original Articles

Upregulation of miR-92a contributes to blocking goblet cell metaplasia by targeting MUC5AC in asthma

, , , & ORCID Icon
Pages 613-619 | Received 05 Nov 2019, Accepted 08 Jun 2020, Published online: 22 Jun 2020
 

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.

Disclosure statement

All authors state that there is no competing interest relationship between them.

Additional information

Funding

This work was supported by funds from the Health Bureau of Zhejiang Province [2017KY191, 2018KY189, and 2020KY003], Natural Science Foundation of Zhejiang Province [LY18H040010], and Zhejiang Provincial Administration of Traditional Chinese Medicine [2020ZB002].

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