Cargando…
MicroRNA‐186 is associated with hypoxia‐inducible factor‐1α expression in chronic obstructive pulmonary disease
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 obs...
Autores principales: | , , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6418446/ https://www.ncbi.nlm.nih.gov/pubmed/30575333 http://dx.doi.org/10.1002/mgg3.531 |
Sumario: | 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. |
---|