ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
Ca2+ entry via alpha1G and TRPV4 channels differentially regulates surface expression of P-selectin and barrier integrity in pulmonary capillary endothelium.
Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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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.
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Who cites it
51 citing papers in PubMed, 91 citations in OpenAlex.
- Voltage-Dependent Ion Channels in Vascular Endothelial Cells: An Unexpected Signaling Pathway in Non-Excitable Cells.Biomedicines · 2026Review
- Calcium channel blocker-associated pulmonary toxicity: epidemiology, mechanisms, and clinical management.Frontiers in pharmacology · 2026Review
- Defective CFTR modulates mechanosensitive channels TRPV4 and PIEZO1 and drives endothelial barrier failure.iScience · 2024Article
- Pulmonary Vascular Dysfunctions in Cystic Fibrosis.Physiology (Bethesda, Md.) · 2024Review
- Lung endothelium, tau, and amyloids in health and disease.Physiological reviews · 2024Review
- Review
- CaCells · 2021Review
- A venous-specific purinergic signaling cascade initiated by Pannexin 1 regulates TNFα-induced increases in endothelial permeability.Science signaling · 2021Article
- A rapid dynamic in vivo near-infrared fluorescence imaging assay to track lung vascular permeability after acute radiation injury.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- TRPV4 channel activation induces the transition of venous and arterial endothelial cells toward a pro-inflammatory phenotype.Physiological reports · 2021Article
- Platelet-derived microvesicles induce calcium oscillations and promote VSMC migrationTheranostics · 2021Article
- TRPV4: A Physio and Pathophysiologically Significant Ion Channel.International journal of molecular sciences · 2020Review
- Endothelial Cell Calcium Signaling during Barrier Function and Inflammation.The American journal of pathology · 2020Review
- Endothelial TRPV4 channels and vasodilator reactivity.Current topics in membranes · 2020Review
- Differential modulation of transendothelial electrical resistance by TRPV4 agonists is mediated by apoptosis and/or necrosis.Biochemistry and biophysics reports · 2019Article
- Transient Receptor Potential Channels and Endothelial Cell Calcium Signaling.Comprehensive Physiology · 2019Review
- αAmerican journal of physiology. Cell physiology · 2019Article
- Modulators of Transient Receptor Potential (TRP) Channels as Therapeutic Options in Lung Disease.Pharmaceuticals (Basel, Switzerland) · 2019Review
- Loss of barrier integrity in alveolar epithelial cells downregulates ENaC expression and activity via CaPflugers Archiv : European journal of physiology · 2018Article
- When higher cholesterol is better: membrane cholesterol loss and endothelial CaAmerican journal of physiology. Heart and circulatory physiology · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Pulmonary vascular endothelial cells express a variety of ion channels that mediate Ca(2+) influx in response to diverse environmental stimuli. However, it is not clear whether Ca(2+) influx from discrete ion channels is functionally coupled to specific outcomes. Thus we conducted a systematic study in mouse lung to address whether the alpha(1G) T-type Ca(2+) channel and the transient receptor potential channel TRPV4 have discrete functional roles in pulmonary capillary endothelium. We used real-time fluorescence imaging for endothelial cytosolic Ca(2+), immunohistochemistry to probe for surface expression of P-selectin, and the filtration coefficient to specifically measure lung endothelial permeability. We demonstrate that membrane depolarization via exposure of pulmonary vascular endothelium to a high-K(+) perfusate induces Ca(2+) entry into alveolar septal endothelial cells and exclusively leads to the surface expression of P-selectin. In contrast, Ca(2+) entry in septal endothelium evoked by the selective TRPV4 activator 4alpha-phorbol-12,13-didecanoate (4alpha-PDD) specifically increases lung endothelial permeability without effect on P-selectin expression. Pharmacological blockade or knockout of alpha(1G) abolishes depolarization-induced Ca(2+) entry and surface expression of P-selectin but does not prevent 4alpha-PDD-activated Ca(2+) entry and the resultant increase in permeability. Conversely, blockade or knockout of TRPV4 specifically abolishes 4alpha-PDD-activated Ca(2+) entry and the increase in permeability, while not impacting depolarization-induced Ca(2+) entry and surface expression of P-selectin. We conclude that in alveolar septal capillaries Ca(2+) entry through alpha(1G) and TRPV4 channels differentially and specifically regulates the transition of endothelial procoagulant phenotype and barrier integrity, respectively.
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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.