ArticleInternational journal of chronic obstructive pulmonary disease2020
MiR-218 Inhibits CSE-Induced Apoptosis and Inflammation in BEAS-2B by Targeting BRD4.
Article in International journal of chronic obstructive pulmonary disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- The Role of MicroRNAs Implicated in the Regulation of PI3K/AKT and Focal Adhesion Signaling Pathways in Chronic Obstructive Pulmonary Disease.Biochemical genetics · 2026Article
- Review
- A novel circular RNA circ_0020647 promotes ETEC-induced IPEC-J2 cell pyroptosis via the ssc-miR-185/BRD4 axis.Frontiers in veterinary science · 2025Article
- Unlocking the secrets of aging: Epigenetic reader BRD4 as the target to combatting aging-related diseases.Journal of advanced research · 2024Review
- BRD4: an effective target for organ fibrosis.Biomarker research · 2024Review
- BRD4 as a Therapeutic Target in Pulmonary Diseases.International journal of molecular sciences · 2023Review
- Ginseng Saponin Rb1 Attenuates Cigarette Smoke Exposure-Induced Inflammation, Apoptosis and Oxidative Stress via Activating Nrf2 and Inhibiting NF-κB Signaling Pathways.International journal of chronic obstructive pulmonary disease · 2023Article
- Regulatory roles of external cholesterol in human airway epithelial mitochondrial function through STARD3 signalling.Clinical and translational medicine · 2022Article
- Inhibition of BRD4 inhibits proliferation and promotes apoptosis of psoriatic keratinocytes.Biomedical engineering online · 2021Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Chronic obstructive pulmonary disease (COPD) is an age-related disease, and its incidence rate is increasing every year. MicroRNAs (miRNAs) play critical roles in the COPD process and function as key biomarkers or potential therapeutic targets for patients with COPD. However, the potential roles and functional effects of miR-218 in COPD remain undefined. Methods: The expression levels of miR-218 and bromodomain protein 4 (BRD4) were assessed by real-time quantitative polymerase chain reaction (RT-qPCR) or Western blot, respectively. In addition, a COPD cell model was established using cigarette smoke extract (CSE) in bronchial epithelial cell line (BEAS-2B). Enzyme-linked immunosorbent assay (ELISA) kit was applied to measure the concentrations of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-8 (IL-8) in cell supernatants of BEAS-2B cells. Moreover, cell apoptosis was examined by flow cytometry assay. The association relationship between miR-218 and BRD4 was confirmed by dual-luciferase reporter and RNA immunoprecipitation assay. Results: MiR-218 was downregulated in COPD and CSE-induced BEAS-2B cells, and it was positively correlated with forced expiratory volume in 1 second (FEV1) % in COPD patients. Mechanically, overexpression of miR-218 or knockdown of BRD4 mitigated apoptosis and inflammation in BEAS-2B cells induced by CSE. Additionally, overexpression of BRD4 weakened the miR-218-mediated effects on CSE-induced BEAS-2B cells. Conclusion: Overexpression of miR-218 inhibited CSE-induced apoptosis and inflammation in BEAS-2B cells by targeting BRD4 expression.
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