ArticleInternational journal of chronic obstructive pulmonary disease2017
Repression of Toll-like receptor-4 by microRNA-149-3p is associated with smoking-related COPD.
Article in International journal of chronic obstructive pulmonary disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 55 citations in OpenAlex.
- Article
- MicroRNAs as promising drug delivery target to ameliorate chronic obstructive pulmonary disease using nano-carriers: a comprehensive review.Molecular and cellular biochemistry · 2025Review
- Targeting toll-like receptors: unveiling potential therapeutic strategies for deep vein thrombosis.Frontiers in immunology · 2025Review
- Epigenetic regulation of macrophage activation in chronic obstructive pulmonary disease.Frontiers in immunology · 2024Review
- The regulatory role of differential microRNA expressions on cellular inflammatory factors IL-6 and IL-10 in Echinococcus granulosus-induced anaphylaxis.Immunity, inflammation and disease · 2023Article
- Lung microRNAs Expression in Lung Cancer and COPD: A Preliminary Study.Biomedicines · 2023Article
- The role of HMGB1/RAGE/TLR4 signaling pathways in cigarette smoke-induced inflammation in chronic obstructive pulmonary disease.Immunity, inflammation and disease · 2022Review
- ISGylation is induced in neurons by demyelination driving ISG15-dependent microglial activation.Journal of neuroinflammation · 2022Article
- Joint detection of miR-149-3p and hepcidin predicts the onset of obstructive sleep apnea syndrome in obese patients.Laryngoscope investigative otolaryngology · 2022Article
- Epigenetic Mechanisms in Parenchymal Lung Diseases: Bystanders or Therapeutic Targets?International journal of molecular sciences · 2022Review
- Transcription Factor p300 Regulated miR-451b Weakens the Cigarette Smoke Extract-Induced Cellular Stress by Targeting RhoA/ROCK2 Signaling.Oxidative medicine and cellular longevity · 2022Article
- Association of toll-like receptors polymorphisms with COPD risk in Chinese population.Frontiers in genetics · 2022Article
- Peripheral Blood Mononuclear Cell Gene Expression in Chronic Obstructive Pulmonary Disease: miRNA and mRNA Regulation.Journal of inflammation research · 2022Article
- The Novel Regulatory Role of the lncRNA-miRNA-mRNA Axis in Chronic Inflammatory Airway Diseases.Frontiers in molecular biosciences · 2022Review
- Long non-coding RNA maternally expressed gene regulates cigarette smoke extract induced lung inflammation and human bronchial epithelial apoptosis via miR-149-3p.Experimental and therapeutic medicine · 2021Article
- Role of Non-Coding RNAs in Post-Transcriptional Regulation of Lung Diseases.Frontiers in genetics · 2021Review
- Mechanisms of the lipopolysaccharide-induced inflammatory response in alveolar epithelial cell/macrophage co-culture.Experimental and therapeutic medicine · 2020Article
- miRNAs in Lung Development and Diseases.International journal of molecular sciences · 2020Review
- MicroRNAs as Potential Regulators of Immune Response Networks in Asthma and Chronic Obstructive Pulmonary Disease.Frontiers in immunology · 2020Review
- Transplacental Innate Immune Training via Maternal Microbial Exposure: Role of XBP1-ERN1 Axis in Dendritic Cell Precursor Programming.Frontiers in immunology · 2020Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSmoking is the leading cause of COPD. Exploring molecular markers and understanding the pathogenic mechanisms of smoking-related COPD are helpful for early clinical diagnosis and treatment of the disease. This study aims to identify specific circulating microRNAs (miRNAs) from the blood of COPD patients with a long history of smoking.
methodsBlood samples from four different groups were collected, and miRNA microarray was performed. Differential expression of miRNAs was verified by quantitative polymerase chain reaction. In vitro, THP-1 cells were cultured and stimulated with cigarette smoke extract (CSE) or transfected with miR-149-3p inhibitor/mimics. Protein levels of Toll-like receptor 4 (TLR-4) and nuclear factor κB (NF-κB) were detected using Western blot and immunofluorescence. Interleukin (IL)-1β and tumor necrosis factor (TNF)-α levels were determined by an enzyme-linked immunosorbent assay.
resultsmiRNA profiling revealed that the expression of 56 miRNAs was changed between the four groups. Expression of miR-149-3p in group C (non-smoker non-COPD) was higher than in group S (smoker non-COPD), S-COPD (smoker with stable COPD) and AE-COPD (smoker with acute exacerbation COPD). CSE stimulation down-regulated the expression of miR-149-3p and up-regulated the TLR-4 and NF-κB levels in THP-1 cells. Transfecting miR-149-3p inhibitors in THP-1 cells also increased the expression of its target genes. Furthermore, overexpression of miR-149-3p inhibited the TLR-4/NF-κB signaling pathways and reduced the secretion of IL-1β and TNF-α.
conclusionThis study found that smoking can induce differential expression of circulating miR-NAs, such as down-regulation of miR-149-3p. Reducing miR-149-3p may increase the inflammatory response in COPD patients through the regulation of the TLR-4/NF-κB signaling pathway.
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