ArticleEnvironmental health perspectives2011
TRPV4-mediated calcium influx into human bronchial epithelia upon exposure to diesel exhaust particles.
Article in Environmental health perspectives, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 123 citations in OpenAlex.
- Modulation of TRPV-1 by prostaglandin-EScientific reports · 2020Trial
- Transient receptor potential vanilloid 4 (TRPV4) channels mediate pulmonary surfactant protein A and D secretion.American journal of respiratory cell and molecular biology · 2026Article
- 25+ Years of TRPV4: From Discovery to Translational Horizons.Research square · 2026Article
- Integration of cAMP and TRPV4 Signaling to Optimize Collagen Remodeling for Management of Fibrosis.Cells · 2025Review
- Respiratory Ciliary Beat Frequency in COPD: Balancing Oxidative Stress and Pharmacological Treatment.Antioxidants (Basel, Switzerland) · 2025Review
- Moderately severe osteogenesis imperfecta-like osteochondrodysplasia associated with heterozygous variants in bothJBMR plus · 2025Article
- Occupational exposure and its mechanistic link to allergic asthma and lung function decline; a data-driven approach coupled to mining of adverse outcome pathway signatures.Frontiers in toxicology · 2025Article
- Regulation of Airway Epithelial-Derived Alarmins in Asthma: Perspectives for Therapeutic Targets.Biomedicines · 2024Review
- TRPV4 Channel Modulators as Potential Drug Candidates for Cystic Fibrosis.International journal of molecular sciences · 2024Review
- Identification and Properties of TRPV4 Mutant Channels Present in Polycystic Kidney Disease Patients.Function (Oxford, England) · 2024Article
- Subacute Exposure to Gaseous Pollutants from Diesel Engine Exhaust Attenuates Capsaicin-Induced Cardio-Pulmonary Reflex Responses Involving Oxidant Stress Mechanisms in Adult Wistar Rats.Cardiovascular toxicology · 2024Article
- TRPV4 Activation during Guinea Pig Airway Smooth Muscle Contraction Promotes CaPharmaceuticals (Basel, Switzerland) · 2024Article
- Respiratory Syncytial Virus Infection Does Not Induce Epithelial-Mesenchymal Transition.Journal of virology · 2023Article
- Bidirectional TRP/L Type CaBiomolecules · 2023Article
- Unconventional interactions of the TRPV4 ion channel with beta-adrenergic receptor ligands.Life science alliance · 2023Article
- Review
- Nicotinic Acid Adenine Dinucleotide Phosphate Induces Intracellular CaFrontiers in cell and developmental biology · 2022Article
- Thermosensory Transient Receptor Potential Ion Channels and Asthma.Biomedicines · 2021Review
- CaCells · 2021Review
- TRP Channels as Cellular Targets of Particulate Matter.International journal of molecular sciences · 2021Review
12 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundHuman respiratory epithelia function in airway mucociliary clearance and barrier function and have recently been implicated in sensory functions.
objectiveWe investigated a link between chronic obstructive pulmonary disease (COPD) pathogenesis and molecular mechanisms underlying Ca2+ influx into human airway epithelia elicited by diesel exhaust particles (DEP). METHODS AND
resultsUsing primary cultures of human respiratory epithelial (HRE) cells, we determined that these cells possess proteolytic signaling machinery, whereby proteinase-activated receptor-2 (PAR-2) activates Ca2+-permeable TRPV4, which leads to activation of human respiratory disease-enhancing matrix metalloproteinase-1 (MMP-1), a signaling cascade initiated by diesel exhaust particles (DEP), a globally relevant air pollutant. Moreover, we observed ciliary expression of PAR-2, TRPV4, and phospholipase-Cβ3 in human airway epithelia and their DEP-enhanced protein-protein complex formation. We also found that the chronic obstructive pulmonary disease (COPD)-predisposing TRPV4P19S variant enhances Ca2+ influx and MMP 1 activation, providing mechanistic linkage between man-made air pollution and human airway disease.
conclusionDEP evoked protracted Ca2+ influx via TRPV4, enhanced by the COPD-predisposing human genetic polymorphism TRPV4P19S. This mechanism reprograms maladaptive inflammatory and extracellular-matrix-remodeling responses in human airways. The novel concept of air pollution-responsive ciliary signal transduction from PAR-2 to TRPV4 in human respiratory epithelia will accelerate rationally targeted therapies, possibly via the inhalatory route.
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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.