ArticleThe Journal of physiology2005
Disruption of CFTR chloride channel alters mechanical properties and cAMP-dependent Cl- transport of mouse aortic smooth muscle cells.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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
36 citing papers in PubMed, 82 citations in OpenAlex.
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- The Role of Ion Channels in Pulmonary Hypertension: A Review.Pulmonary circulation · 2025Review
- Cystic Fibrosis: Understanding Cystic Fibrosis Transmembrane Regulator Mutation Classification and Modulator Therapies.Advances in respiratory medicine · 2024Review
- Pulmonary Vascular Dysfunctions in Cystic Fibrosis.Physiology (Bethesda, Md.) · 2024Review
- The long-term effect of elexacaftor/tezacaftor/ivacaftor on cardiorespiratory fitness in adolescent patients with cystic fibrosis: a pilot observational study.BMC pulmonary medicine · 2024Observational
- CFTR dysfunction in smooth muscle drives TGFβ dependent airway hyperreactivity.Respiratory research · 2023Article
- Genome Editing for Cystic Fibrosis.Cells · 2023Review
- Ventilatory Threshold and Risk of Pulmonary Exacerbations in Cystic Fibrosis.Respiratory care · 2023Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- The Pleiotropic Role of Extracellular ATP in Myocardial Remodelling.Molecules (Basel, Switzerland) · 2023Review
- Elexacaftor-Tezacaftor-Ivacaftor improves exercise capacity in adolescents with cystic fibrosis.Pediatric pulmonology · 2022Article
- CFTR Suppresses Neointimal Formation Through Attenuating Proliferation and Migration of Aortic Smooth Muscle Cells.Journal of cardiovascular pharmacology · 2022Article
- Cystic Fibrosis Human Organs-on-a-Chip.Micromachines · 2021Review
- CF airway smooth muscle transcriptome reveals a role for PYK2.JCI insight · 2017Article
- Cystic Fibrosis Transmembrane Conductance Regulator in Sarcoplasmic Reticulum of Airway Smooth Muscle. Implications for Airway Contractility.American journal of respiratory and critical care medicine · 2016Article
- Genetic Regulation of Endothelial Vasomotor Function.Frontiers in physiology · 2016Review
- Regulation of vascular tone and arterial blood pressure: role of chloride transport in vascular smooth muscle.Pflugers Archiv : European journal of physiology · 2015Review
- Genotype-specific alterations in vascular smooth muscle cell function in cystic fibrosis piglets.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2014Article
- Cl⁻ channels in smooth muscle cells.Pflugers Archiv : European journal of physiology · 2014Review
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chloride (Cl(-)) channels expressed in vascular smooth muscle cells (VSMC) are important to control membrane potential equilibrium, intracellular pH, cell volume maintenance, contraction, relaxation and proliferation. The present study was designed to compare the expression, regulation and function of CFTR Cl(-) channels in aortic VSMC from Cftr(+/+) and Cftr(-)(/)(-) mice. Using an iodide efflux assay we demonstrated stimulation of CFTR by VIP, isoproterenol, cAMP agonists and other pharmacological activators in cultured VSMC from Cftr(+/+). On the contrary, in cultured VSMC from Cftr(-)(/)(-) mice these agonists have no effect, showing that CFTR is the dominant Cl(-) channel involved in the response to cAMP mediators. Angiotensin II and the calcium ionophore A23187 stimulated Ca(2)(+)-dependent Cl(-) channels in VSMCs from both genotypes. CFTR was activated in myocytes maintained in medium containing either high potassium or 5-hydroxytryptamine (5-HT) and was inhibited by CFTR(inh)-172, glibenclamide and diphenylamine-2,2'-dicarboxylic acid (DPC). We also examined the mechanical properties of aortas. Arteries with or without endothelium from Cftr(-/-) mice became significantly more constricted (approximately 2-fold) than that of Cftr(+/+) mice in response to vasoactive agents. Moreover, in precontracted arteries of Cftr(+/+) mice, VIP and CFTR activators induced vasorelaxation that was altered in Cftr(-/-) mice. Our findings suggest a novel mechanism for regulation of the vascular tone by cAMP-dependent CFTR chloride channels in VSMC. To our knowledge this study is the first to report the phenotypic consequences of the loss of a Cl(-) channel on vascular reactivity.
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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.