ArticleBioscience reports2020
LncRNA MIR155HG contributes to smoke-related chronic obstructive pulmonary disease by targeting miR-128-5p/BRD4 axis.
Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- Review
- Long noncoding RNAs at the crossroads of smoking, oxidative stress, inflammation, and lung disease.Archives of toxicology · 2026Review
- Diagnostic and prognostic value of serum miR-155 in chronic obstructive pulmonary disease.Scientific reports · 2026Article
- Exploring the Roles of Wnt Signaling Pathway and Non-Coding RNAs in COPD.International journal of chronic obstructive pulmonary disease · 2026Review
- LncRNA MIR155HG suppresses cell apoptosis by activating autophagy via miR-7036b-3p/GPNMB axis and AMPK/mTOR signaling in spinal cord injury.Non-coding RNA research · 2025Article
- Orchestrating inflammation: non-coding RNAs as master regulators of macrophage function in chronic obstructive pulmonary disease-an update.Frontiers in immunology · 2025Review
- Long non-coding RNA Small Nucleolar RNA Host Gene 4 ameliorates cigarette smoke-induced proliferation, apoptosis, inflammation, and airway remodeling in alveolar epithelial cells through the modulation of the mitogen-activated protein kinase signaling pathway via the microRNA-409-3p/Four and a Half LIM Domains 1 axis.European journal of medical research · 2024Article
- Functional roles of circular RNAs in lung injury.Frontiers in pharmacology · 2024Review
- Review
- BRD4 as a Therapeutic Target in Pulmonary Diseases.International journal of molecular sciences · 2023Review
- MEG3 Regulates CSE-Induced Apoptosis by Regulating miR-421/DFFB Signal Axis.International journal of chronic obstructive pulmonary disease · 2023Article
- Article
- MicroRNA Control Lipid-laden Alveolar Macrophages in Smokers: A Potential Therapeutic Target for Chronic Obstructive Pulmonary Disease?American journal of respiratory cell and molecular biology · 2022Article
- Long noncoding RNAActa biochimica et biophysica Sinica · 2022Article
- LncRNA MIR155HG functions as a ceRNA of miR-223-3p to promote cell pyroptosis in human degenerative NP cells.Clinical and experimental immunology · 2022Article
- Involvement ofAnnals of translational medicine · 2022Article
- The Novel Regulatory Role of the lncRNA-miRNA-mRNA Axis in Chronic Inflammatory Airway Diseases.Frontiers in molecular biosciences · 2022Review
- The roles of long noncoding RNA-mediated macrophage polarization in respiratory diseases.Frontiers in immunology · 2022Review
- lncRNA-NEAT1 Sponges miR-128 to Promote Inflammatory Reaction and Phenotypic Transformation of Airway Smooth Muscle Cells.Computational and mathematical methods in medicine · 2022Article
- Review
Corrections and comments
- Expression of concern
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic obstructive pulmonary disease (COPD) is a common airway disease characterized by an exaggerated pulmonary inflammatory response. Long noncoding MIR155 host gene (lncRNA MIR155HG) has been identified to be related to the macrophage polarization in COPD. However, the detailed function of MIR155HG in cigarette smoke (CS)-mediated COPD remains largely unknown. The expression level of MIR155HG was elevated while miR-218-5p was decreased in lung tissues of smokers without or with COPD, especially in smokers with COPD, and cigarette smoke extract (CSE)-treated human pulmonary microvascular endothelial cell (HPMECs) in a dose- and time-dependent manner. Then, functional experiments showed that MIR155HG deletion could reverse CSE exposure-induced apoptosis and inflammation in HPMECs. MiR-218-5p was confirmed to be a target of MIR155HG and rescue assay showed miR-218-5p inhibitor attenuated the inhibitory action of MIR155HG knockdown on CSE-induced HPMECs. Subsequently, miR-218-5p was found to target bromodomain containing 4 (BRD4) directly, and miR-218-5p overexpression overturned CSE-induced injury of HPMECs via regulating BRD4. Additionally, co-expression analysis indicated MIR155HG indirectly regulated BRD4 expression in HPMECs via miR-218-5p. Thus, we concluded that MIR155HG contributed to the apoptosis and inflammation of HPMECs in smoke-related COPD by regulating miR-128-5p/BRD4 axis, providing a novel insight on the pathogenesis of COPD and a therapeutic strategy on COPD treatments.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.