Open AccessMicroRNA‐186 is associated with hypoxia‐inducible factor‐1α expression in chronic obstructive pulmonary disease
Author(s) -
Lin Li,
Sun Juan,
Wu Duoyi,
Lin Daobo,
Sun Dingwei,
Li Quanni,
Chen Jiannan,
Niu Huan,
He Ping,
Ding Yipeng
Publication year - 2019
Publication title -
molecular genetics and genomic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.765
H-Index - 29
ISSN - 2324-9269
DOI - 10.1002/mgg3.531
Subject(s) - microrna , transfection , copd , flow cytometry , biology , apoptosis , cancer research , viability assay , pathogenesis , microbiology and biotechnology , cell culture , immunology , medicine , gene , genetics
Background MicroRNAs (miRNAs) are a family of small noncoding RNAs and are essential in the regulation of gene expression. Their impacts on gene expression have been reported in various diseases. The role of hypoxia‐inducible factor 1 alpha (HIF‐1α) in the development and progression of chronic obstructive pulmonary disease (COPD) has also been demonstrated. However, the role of microRNA‐186 (miR‐186) in relation to HIF in COPD is unknown. Methods Cell culture experiments were performed using human lung fibroblast cells (MRC‐5). Cell viability was determined by MTT and flow cytometry assays. Reverse transcriptase‐polymerase chain reaction (RT‐PCR) and Western blot analysis were used to assess the expression levels of HIF‐1α and inflammatory cytokines. Dual‐luciferase reporter assays were used to reveal the correlation between miR‐186 and HIF‐1α. Results After miR‐186 transfection, the cell lines showed reduced proliferation and increased apoptosis. After overexpression of miR‐186, we found that the HIF‐1α expression level was reduced in MRC‐5 cells. We found that miR‐186 can affect apoptosis of inflammatory fibroblasts through the regulation of HIF‐1α and affect the downstream signaling pathways. Conclusions These data suggested that miR‐186 contributes to the pathogenesis of COPD and that miRNA‐186 may also affect the HIF‐1α‐dependent lung structure maintenance program.