ArticleThe Journal of biological chemistry2008
The aryl hydrocarbon receptor attenuates tobacco smoke-induced cyclooxygenase-2 and prostaglandin production in lung fibroblasts through regulation of the NF-kappaB family member RelB.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
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Who cites it
96 citing papers in PubMed, 149 citations in OpenAlex.
- Aryl hydrocarbon receptor (AhR) regulates organic dust and organic dust-associated bacterial extracellular vesicles-induced airway inflammation via ROS-dependent NFκB and STAT3 activation.Respiratory research · 2026Article
- AhR as a Common Denominator in Immunity and Inflammation in Chronic Lung Diseases: Molecular and Clinical Insights.Diseases (Basel, Switzerland) · 2026Review
- Compartmental analysis of the pulmonary proteome reveals novel functions of the aryl hydrocarbon receptor.Respiratory research · 2026Article
- The Role of Aryl Hydrocarbon Receptor in Airway Remodeling: Mechanistic Insights Across Cellular Functions.Clinical reviews in allergy & immunology · 2026Review
- Indirubin regulates M1/M2 polarization and inhibits ferroptosis in dextran sulfate sodium induced colitis and in cultured THP-1 cells.Pharmaceutical biology · 2025Article
- Cytochrome P450 (CYP) 1 enzymes in acute lung injury: from molecular insights to therapeutic implications.Redox report : communications in free radical research · 2025Review
- The AhR Is a Critical Regulator of the Pulmonary Response to Cannabis Smoke.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- New insights into coordinated regulation of AHR promoter transcription; molecular mechanisms and therapeutic targets.International journal of biological sciences · 2025Review
- Kynurenic Acid/AhR Signaling at the Junction of Inflammation and Cardiovascular Diseases.International journal of molecular sciences · 2024Review
- Deciphering NF-kappaB pathways in smoking-related lung carcinogenesis.EXCLI journal · 2024Review
- Paroxetine protects against bleomycin-induced pulmonary fibrosis by blocking GRK2/Smad3 pathway.Aging · 2023Article
- Animal models of drug-induced pulmonary fibrosis: an overview of molecular mechanisms and characteristics.Cell biology and toxicology · 2022Review
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- The Aryl Hydrocarbon Receptor (AHR): A Novel Therapeutic Target for Pulmonary Diseases?International journal of molecular sciences · 2022Review
- More than Meets the Eye: The Aryl Hydrocarbon Receptor is an Environmental Sensor, Physiological Regulator and a Therapeutic Target in Ocular Disease.Frontiers in toxicology · 2022Review
- Standardized Cannabis Smoke Extract Induces Inflammation in Human Lung Fibroblasts.Frontiers in pharmacology · 2022Article
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- 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
36 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Diseases such as chronic obstructive pulmonary disease and lung cancer caused by cigarette smoke affect millions of people worldwide. The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that influences responses to certain environmental pollutants such as tobacco smoke. However, the physiological function(s) of the AhR is unknown. Herein we propose that the physiologic role of the AhR is to limit inflammation. We show that lung fibroblasts from AhR(-/-) mice produce a heightened inflammatory response to cigarette smoke, typified by increased levels of cyclooxygenase-2 (COX-2) and prostaglandins (PGs), when compared with wild type (AhR(+/+)) fibroblasts. This response was dependent on AhR expression as transient transfection of an AhR expression plasmid into AhR(-/-) fibroblasts significantly attenuated the smoke-induced COX-2 and PG production, confirming the anti-inflammatory role of the AhR. The AhR can interact with NF-kappaB. However, the heightened inflammatory response observed in AhR(-/-) fibroblasts was not the result of NF-kappaB (p50/p65) activation. Instead it was coupled with a loss of the NF-kappaB family member RelB in AhR(-/-) fibroblasts. Taken together, these studies provide compelling evidence that AhR expression limits proinflammatory COX-2 and PG production by maintaining RelB expression. The association between RelB and AhR may represent a new therapeutic and more selective target with which to combat inflammation-associated diseases.
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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.