ArticleRespiratory research2015
Decreased expression of the NF-κB family member RelB in lung fibroblasts from Smokers with and without COPD potentiates cigarette smoke-induced COX-2 expression.
Article in Respiratory research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 30 citations in OpenAlex.
- Cigarette smoke extract exposure induces gut microbial dysbiosis and impairs short-chain fatty acid metabolism in juvenile rats.Pediatric research · 2026Article
- AhR as a Common Denominator in Immunity and Inflammation in Chronic Lung Diseases: Molecular and Clinical Insights.Diseases (Basel, Switzerland) · 2026Review
- Dysregulation of Arachidonic Acid Metabolism Drives Inflammatory Lipid Production in Localized Provoked Vulvodynia.Nutrients · 2025Article
- Bilirubin regulates cell death type by alleviating macrophage mitochondrial dysfunction caused by cigarette smoke extract.Redox report : communications in free radical research · 2024Article
- Erythromycin regulates peroxisome proliferator-activated receptor γ to ameliorate cigarette smoke-induced oxidative stress in macrophages.Journal of thoracic disease · 2024Article
- EPC-exosomal miR-26a-5p improves airway remodeling in COPD by inhibiting ferroptosis of bronchial epithelial cells via PTGS2/PGE2 signaling pathway.Scientific reports · 2023Article
- From Nucleus to Organs: Insights of Aryl Hydrocarbon Receptor Molecular Mechanisms.International journal of molecular sciences · 2022Review
- The Aryl Hydrocarbon Receptor (AHR): A Novel Therapeutic Target for Pulmonary Diseases?International journal of molecular sciences · 2022Review
- Aberrant Post-Transcriptional Regulation of Protein Expression in the Development of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2021Review
- Human antigen R promotes lung fibroblast differentiation to myofibroblasts and increases extracellular matrix production.Journal of cellular physiology · 2021Article
- Aryl hydrocarbon receptor deficiency causes the development of chronic obstructive pulmonary disease through the integration of multiple pathogenic mechanisms.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Angiotensin-converting enzyme 2 expression in COPD and IPF fibroblasts: the forgotten cell in COVID-19.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Mechanism of Action of Bu-Fei-Yi-Shen Formula in Treating Chronic Obstructive Pulmonary Disease Based on Network Pharmacology Analysis and Molecular Docking Validation.BioMed research international · 2020Article
- Bufei Jianpi Formula Improves Mitochondrial Function and Suppresses Mitophagy in Skeletal Muscle via the Adenosine Monophosphate-Activated Protein Kinase Pathway in Chronic Obstructive Pulmonary Disease.Frontiers in pharmacology · 2020Article
- The Aryl Hydrocarbon Receptor and the Maintenance of Lung Health.International journal of molecular sciences · 2018Review
- Regional heterogeneity in response of airway epithelial cells to cigarette smoke.BMC pulmonary medicine · 2018Article
- Over-expression of nuclear factor-κB family genes and inflammatory molecules is related to chronic obstructive pulmonary disease.International journal of chronic obstructive pulmonary disease · 2018Article
- Inhaled Pollutants: The Molecular Scene behind Respiratory and Systemic Diseases Associated with Ultrafine Particulate Matter.International journal of molecular sciences · 2017Review
- Aryl hydrocarbon receptor (AhR)-dependent regulation of pulmonary miRNA by chronic cigarette smoke exposure.Scientific reports · 2017Article
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundHeightened inflammation, including expression of COX-2, is associated with COPD pathogenesis. RelB is an NF-κB family member that attenuates COX-2 in response to cigarette smoke by a mechanism that may involve the miRNA miR-146a. There is no information on the expression of RelB in COPD or if RelB prevents COX-2 expression through miR-146a.
methodsRelB, Cox-2 and miR-146a levels were evaluated in lung fibroblasts and blood samples derived from non-smokers (Normal) and smokers (At Risk) with and without COPD by qRT-PCR. RelB and COX-2 protein levels were evaluated by western blot. Human lung fibroblasts from Normal subjects and smokers with and without COPD, along with RelB knock-down (siRNA) in Normal cells, were exposed to cigarette smoke extract (CSE) in vitro and COX-2 mRNA/protein and miR-146a levels assessed.
resultsBasal expression of RelB mRNA and protein were significantly lower in lung cells derived from smokers with and without COPD, the latter of which expressed more Cox-2 mRNA and protein in response to CSE. Knock-down of RelB in Normal fibroblasts increased Cox-2 mRNA and protein induction by CSE. Basal miR-146a levels were not different between the three groups, and only Normal fibroblasts increased miR-146a expression in response to smoke. There was a positive correlation between systemic RelB and Cox-2 mRNA levels and circulating miR-146a levels were higher only in GOLD stage I subjects.
conclusionsOur data indicate that RelB attenuates COX-2 expression in lung structural cells, such that loss of pulmonary RelB may be an important determinant in the aberrant, heightened inflammation associated with COPD pathogenesis.
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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.