ArticleJournal of thoracic disease2019
Role of miRNA-181a-2-3p in cadmium-induced inflammatory responses of human bronchial epithelial cells.
Article in Journal of thoracic disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed.
- Association of miR-146a/b and miR-181a with Chronic Obstructive Pulmonary Disease.Biochemical genetics · 2026Article
- Mapping the MicroRNA Landscape of Cadmium Exposure: A Bibliometric and Bioinformatics Analysis of Molecular Targets and Regulatory Pathways.International journal of molecular sciences · 2026Review
- Diagnostic and Monitoring Potential of Sputum-Derived miRNAs in Patients with Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2026Review
- Nanomaterials in COPD: Emerging Therapeutic and Diagnostic Frontiers with a Focus on Metal-Organic Frameworks.International journal of molecular sciences · 2025Review
- The Protective Effects ofToxics · 2024Article
- Evaluation of penalized and machine learning methods for asthma disease prediction in the Korean Genome and Epidemiology Study (KoGES).BMC bioinformatics · 2024Article
- Low dose cadmium exposure regulates miR-381-ANO1 interaction in airway epithelial cells.Scientific reports · 2024Article
- Differential miRNA Profiling Reveals miR-4433a-5p as a Key Regulator of Chronic Obstructive Pulmonary Disease Progression via PIK3R2- mediated Phenotypic Modulation.Combinatorial chemistry & high throughput screening · 2024Article
- Identification of potential key molecules and signaling pathways for psoriasis based on weighted gene co-expression network analysis.World journal of clinical cases · 2022Article
- Article
- miR-30a targets STOX2 to increase cell proliferation and metastasis in hydatidiform moles via ERK, AKT, and P38 signaling pathways.Cancer cell international · 2022Article
- Identification of epigenetic modifications mediating the antagonistic effect of selenium against cadmium-induced breast carcinogenesis.Environmental science and pollution research international · 2022Article
- Epigenetic Mechanisms in Parenchymal Lung Diseases: Bystanders or Therapeutic Targets?International journal of molecular sciences · 2022Review
- Article
- Targeting Inflammasome Activation in COVID-19: Delivery of RNA Interference-Based Therapeutic Molecules.Biomedicines · 2021Review
- MicroRNA 181a-2-3p Alleviates the Apoptosis of Renal Tubular Epithelial Cells via Targeting GJB2 in Sepsis-Induced Acute Kidney Injury.Molecular and cellular biology · 2021Article
- Epimutational effects of electronic cigarettes.Environmental science and pollution research international · 2021Review
- Gga-miR-181a modulates ANP32A expression and inhibits MDCC-MSB-1 cell.In vitro cellular & developmental biology. Animal · 2021Article
- Non-Coding RNAs in the Transcriptional Network That Differentiates Skeletal Muscles of Sedentary from Long-Term Endurance- and Resistance-Trained Elderly.International journal of molecular sciences · 2021Article
- Long non-coding maternally expressed gene 3 regulates cigarette smoke extract-induced apoptosis, inflammation and cytotoxicity by sponging miR-181a-2-3p in 16HBE cells.Oncology letters · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInflammation is an important priming event in the pathogenesis of pulmonary diseases, including chronic obstructive pulmonary disease (COPD). Increasing evidence indicates that microRNAs (miRNAs) contribute to the pathogenesis of COPD by regulating inflammatory response. Therefore, it is necessary to investigate novel molecular targets in COPD without any validation in COPD samples in airway inflammation. The aim of our study is to reveal novel miRNAs that can influence molecular targets for COPD and to examine the underlying mechanism in airway inflammation.
methodsWe identified the downregulation of miR-181a-2-3p in the serum of COPD patients and further investigated the role of miR-181a-2-3p in cadmium (Cd)-induced inflammation of a human bronchial epithelial cell line (BEAS-2B) and normal human bronchial epithelial (NHBE) cells.
resultsOur results showed that expression of miR-181a-2-3p was significantly decreased in Cd-treated cells and silencing of miR-181a-2-3p enhanced Cd-induced inflammatory responses and inflammasome activation. This negative regulatory effect of miR-181a-2-3p on inflammation is partly mediated by the calcium signaling pathway. Furthermore, global gene expression profiling revealed that Toll-like receptor 4 or sequestosome 1 genes were identified as potential targets of miR-181a-2-3p, which were significantly upregulated by knockdown of miR-181a-2-3p in Cd-treated cells.
conclusionsOur results strongly suggest that miR-181a-2-3p has a critical role in Cd-induced inflammation of airway by regulating its potential target genes, which could be molecular targets for COPD.
Indexed as
Identifiers
What OpenQuestion holds
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.