ArticleMediators of inflammation2015
Lung Epithelial TRPA1 Transduces the Extracellular ROS into Transcriptional Regulation of Lung Inflammation Induced by Cigarette Smoke: The Role of Influxed Ca²⁺.
Article in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 53 citations in OpenAlex.
- TRPA1 Regulates Fibrosis-Associated Transcriptional Pathways in Human Lung Epithelial Cells.Basic & clinical pharmacology & toxicology · 2026Article
- Article
- The TRPA1 cation channel is upregulated by cigarette smoke in mouse and human macrophages modulating lung inflammation.Scientific reports · 2025Article
- The efficacy of ophiopogonanone B in treating the cough in mice infected withFrontiers in pharmacology · 2025Article
- Transient Receptor Potential Ankyrin 1 (TRPA1) Channel Mediates Acrolein Cytotoxicity in Human Lung Cancer Cells.International journal of molecular sciences · 2023Article
- The regulation of TRPA1 expression and function by Th1 and Th2-type inflammation in human A549 lung epithelial cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Curcumin suppresses cell proliferation and reduces cholesterol absorption in Caco-2 cells by activating the TRPA1 channel.Lipids in health and disease · 2023Article
- Inflammation-the role of TRPA1 channel.Frontiers in physiology · 2023Review
- Peripheral Nerve Resident Macrophages and Schwann Cells Mediate Cancer-Induced Pain.Cancer research · 2021Article
- Acute cigarette smoke or extract exposure rapidly activates TRPA1-mediated calcium influx in primary human airway smooth muscle cells.Scientific reports · 2021Article
- Role of TRPA1 in Tissue Damage and Kidney Disease.International journal of molecular sciences · 2021Review
- TRP channels in airway sensory nerves.Neuroscience letters · 2021Review
- Article
- TRP Channels as Cellular Targets of Particulate Matter.International journal of molecular sciences · 2021Review
- Renal Tubular Epithelial TRPA1 Acts as An Oxidative Stress Sensor to Mediate Ischemia-Reperfusion-Induced Kidney Injury through MAPKs/NF-κB Signaling.International journal of molecular sciences · 2021Article
- Cigarette Smoke Promotes Interleukin-8 Production in Alveolar Macrophages Through the Reactive Oxygen Species/Stromal Interaction Molecule 1/CaFrontiers in physiology · 2021Article
- Complex Regulatory Role of the TRPA1 Receptor in Acute and Chronic Airway Inflammation Mouse Models.International journal of molecular sciences · 2020Article
- Lung Epithelial TRPA1 Mediates Lipopolysaccharide-Induced Lung Inflammation in Bronchial Epithelial Cells and Mice.Frontiers in physiology · 2020Article
- Renal Tubular TRPA1 as a Risk Factor for Recovery of Renal Function from Acute Tubular Necrosis.Journal of clinical medicine · 2019Article
- Iron oxide nanoparticles induce reversible endothelial-to-mesenchymal transition in vascular endothelial cells at acutely non-cytotoxic concentrations.Particle and fibre toxicology · 2019Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism underlying the inflammatory role of TRPA1 in lung epithelial cells (LECs) remains unclear. Here, we show that cigarette smoke extract (CSE) sequentially induced several events in LECs. The Ca(2+) influx was prevented by decreasing extracellular reactive oxygen species (ROS) with the scavenger N-acetyl-cysteine, removing extracellular Ca(2+) with the chelator EGTA, or treating with the TRPA1 antagonist HC030031. NADPH oxidase activation was abolished by its inhibitor apocynin, EGTA, or HC030031. The increased intracellular ROS was halted by apocynin, N-acetyl-cysteine, or HC030031. The activation of the MAPKs/NF-κB signaling was suppressed by EGTA, N-acetyl-cysteine, or HC030031. IL-8 induction was inhibited by HC030031 or TRPA1 siRNA. Additionally, chronic cigarette smoke (CS) exposure in wild-type mice induced TRPA1 expression in LECs and lung tissues. In CS-exposure trpa1 (-/-) mice, the increased BALF level of ROS was similar to that of CS-exposure wild-type mice; yet lung inflammation was lessened. Thus, in LECs, CSE may initially increase extracellular ROS, which activate TRPA1 leading to an increase in Ca(2+) influx. The increased intracellular Ca(2+) contributes to activation of NADPH oxidase, resulting in increased intracellular ROS, which activate the MAPKs/NF-κB signaling leading to IL-8 induction. This mechanism may possibly be at work in mice chronically exposed to CS.
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