ArticleJournal of clinical laboratory analysis2021
MiR-221-3p and miR-92a-3p enhances smoking-induced inflammation in COPD.
Article in Journal of clinical laboratory analysis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
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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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Recent Evidences of Epigenetic Alterations in Chronic Obstructive Pulmonary Disease (COPD): A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Trial
- miR-766-5p Attenuates Cigarette Smoke-Induced COPD by Targeting MAPK1.Journal of biochemical and molecular toxicology · 2026Article
- The impact of miR-221-3p modification by the m6A demethylase ALKBH5 on the inflammatory response in spinal tuberculosis and its diagnostic significance.Journal of orthopaedic surgery and research · 2025Article
- Identification of STAT3 signaling as a shared pathogenic signature in systemic lupus erythematosus, chronic obstructive pulmonary disease, and asthma.Scientific reports · 2025Article
- miR-221-3p, arterial blood gas, and lung ultrasound: a multimodal approach for predicting neonatal respiratory distress syndrome outcomes.Journal of cardiothoracic surgery · 2025Article
- Lipopolysaccharide (LPS) induces sclerostin secretion by extracellular vesicle via TLR4/miR-92a-3p/PTEN/NF-κB signalling pathway in murine macrophage.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- MiR-92a-3p Promotes Renal Injury and Fibrosis Through Facilitating M1 Macrophage Polarization via Targeting LIN28A.Physiological research · 2024Article
- Suppressor of cytokine signaling-3 expression and its regulation in relation to inflammation in Chronic Obstructive Pulmonary Disease.Frontiers in immunology · 2024Article
- Differential responses to avian pathogenicFrontiers in cellular and infection microbiology · 2024Article
- Article
- Significant role of circRNA BBS9 in chronic obstructive pulmonary disease via miRNA-103a-3p/BCL2L13.BMC pulmonary medicine · 2023Article
- Treatment of Acute Respiratory Distress Syndrome Caused by COVID-19 with Human Umbilical Cord Mesenchymal Stem Cells.International journal of molecular sciences · 2023Article
- Review
- Seven ferroptosis-specific expressed genes are considered as potential biomarkers for the diagnosis and treatment of cigarette smoke-induced chronic obstructive pulmonary disease.Annals of translational medicine · 2022Article
- Influence of age and sex on microRNA response and recovery in the hippocampus following sepsis.Aging · 2022Article
- MicroRNA-221-3p alleviates cell apoptosis and inflammatory response by targeting cyclin dependent kinase inhibitor 1B in chronic obstructive pulmonary disease.Bioengineered · 2021Article
- MiR-221-3p and miR-92a-3p enhances smoking-induced inflammation in COPD.Journal of clinical laboratory analysis · 2021Article
- The Role of Extracellular Vesicles as a Shared Disease Mechanism Contributing to Multimorbidity in Patients With COPD.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSmoking is likely to facilitate airway inflammation and finally contributes to chronic obstructive pulmonary disease (COPD). This investigation was intended to elucidate miRNAs that were involved in smoking-induced COPD.
methodsAltogether 155 COPD patients and 77 healthy volunteers were recruited, and their serum levels of miR-221-3p and miR-92a-3p were determined. Besides, human bronchial epithelial cells (16HBECs) were purchased, and they were treated by varying concentrations of cigarette smoke extract (CSE). The 16HBECs were, additionally, transfected by miR-221-3p mimic, miR-92a-3p mimic, miR-221-3p inhibitor or miR-92a-3p inhibitor, and cytokines released by them, including TNF-α, IL-8, IL-1β, and TGF-β1, were monitored using enzyme linked immunosorbent assay (ELISA) kits.
resultsChronic obstructive pulmonary disease patients possessed higher serum levels of miR-221-3p and miR-92a-3p than healthy volunteers (p < 0.05), and both miR-221-3p and miR-92a-3p were effective biomarkers in diagnosing stable COPD from acute exacerbation COPD. Moreover, viability of 16HBECs was undermined by CSE treatment (p < 0.05), and exposure to CSE facilitated 16HBECs' release of TNF-α, IL-8, IL-1β, and TGF-β1 (p < 0.05). Furthermore, miR-221-3p/miR-92a-3p expression in 16HBECs was significantly suppressed after transfection of miR-221-3p/miR-92a-3p inhibitor (p < 0.05), which abated CSE-triggered increase in cytokine production and decline in viability of 16HBECs (p < 0.05).
conclusionMiR-221-3p and miR-92a-3p were involved in CSE-induced hyperinflammation of COPD, suggesting that they were favorable alternatives in diagnosing COPD patients with smoking history.
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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 Socratic graph.