ArticlePulmonary circulation2015
Functional coupling of TRPV4, IK, and SK channels contributes to Ca(2+)-dependent endothelial injury in rodent lung.
Article in Pulmonary circulation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- Senicapoc treatment in COVID-19 patients with severe respiratory insufficiency-A randomized, open-label, phase II trial.Acta anaesthesiologica Scandinavica · 2022Trial
- Transient receptor potential vanilloid channels in inflammatory bowel diseases: linking inflammation, angiogenesis, and oxidative stress.Inflammopharmacology · 2026Review
- Lung endothelium, tau, and amyloids in health and disease.Physiological reviews · 2024Review
- Endothelial TRPV4 channels in lung edema and injury.Current topics in membranes · 2022Review
- Restricted Intimal CaFrontiers in physiology · 2022Article
- Augmented KInternational journal of molecular sciences · 2021Article
- Heteromeric TRP Channels in Lung Inflammation.Cells · 2021Review
- Caveolar peroxynitrite formation impairs endothelial TRPV4 channels and elevates pulmonary arterial pressure in pulmonary hypertension.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Treatment with senicapoc in a porcine model of acute respiratory distress syndrome.Intensive care medicine experimental · 2021Article
- Mechanisms underlying selective coupling of endothelial CaThe Journal of physiology · 2020Article
- Ablation of Endothelial TRPV4 Channels Alters the Dynamic CaInternational journal of molecular sciences · 2020Article
- Regulation of Vessel Permeability by TRP Channels.Frontiers in physiology · 2020Review
- Transient Receptor Potential Channels and Endothelial Cell Calcium Signaling.Comprehensive Physiology · 2019Review
- Functional Interaction among KInternational journal of molecular sciences · 2019Review
- Caveolae facilitate TRPV4-mediated CaAmerican journal of physiology. Renal physiology · 2018Article
- Loss of barrier integrity in alveolar epithelial cells downregulates ENaC expression and activity via CaPflugers Archiv : European journal of physiology · 2018Article
- GPR40 is a low-affinity epoxyeicosatrienoic acid receptor in vascular cells.The Journal of biological chemistry · 2018Article
- Hydrogen sulfide-induced vasodilation mediated by endothelial TRPV4 channels.American journal of physiology. Heart and circulatory physiology · 2016Article
- Endothelial SK3 channel-associated Ca2+ microdomains modulate blood pressure.American journal of physiology. Heart and circulatory physiology · 2016Article
- Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Our previous work has shown that the increased lung endothelial permeability response to 14,15-epoxyeicosatrienoic acid (14,15-EET) in rat lung requires Ca(2+) entry via vanilloid type-4 transient receptor potential (TRPV4) channels. Recent studies suggest that activation of TRPV4 channels in systemic vascular endothelium prolongs agonist-induced hyperpolarization and amplifies Ca(2+) entry by activating Ca(2+)-activated K(+) (KCa) channels, resulting in vessel relaxation. Activation of endothelial KCa channels thus has potential to increase the electrochemical driving force for Ca(2+) influx via TRPV4 channels and to amplify permeability responses to TRPV4 activation in lung. To examine this hypothesis, we used Western blot analysis, electrophysiological recordings, and isolated-lung permeability measurements to document expression of TRPV4 and KCa channels and the potential for functional coupling. The results show that rat pulmonary microvascular endothelial cells express TRPV4 and 3 KCa channels of different conductances: large (BK), intermediate (IK), and small (SK3). However, TRPV4 channel activity modulates the IK and SK3, but not the BK, channel current density. Furthermore, the TRPV4-mediated permeability response to 14,15-EET in mouse lung is significantly attenuated by pharmacologic blockade of IK and SK3, but not BK, channels. Collectively, this functional coupling suggests that endothelial TRPV4 channels in rodent lung likely form signaling microdomains with IK and SK3 channels and that the integrated response dictates the extent of lung endothelial injury caused by 14,15-EET.
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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.