ArticlePulmonary circulation
Activity of Ca -activated Cl channels contributes to regulating receptor- and store-operated Ca entry in human pulmonary artery smooth muscle cells.
Article in Pulmonary circulation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- ANO1, CaV1.2, and IP3R form a localized unit of EC-coupling in mouse pulmonary arterial smooth muscle.The Journal of general physiology · 2023Article
- Calcineurin Is a Universal Regulator of Vessel Function-Focus on Vascular Smooth Muscle Cells.Cells · 2023Review
- Pathophysiology and pathogenic mechanisms of pulmonary hypertension: role of membrane receptors, ion channels, and CaPhysiological reviews · 2023Review
- Role of Ion Channel Remodeling in Endothelial Dysfunction Induced by Pulmonary Arterial Hypertension.Biomolecules · 2022Review
- The diverse roles of TMEM16A CaJournal of advanced research · 2021Review
- Halofuginone, a promising drug for treatment of pulmonary hypertension.British journal of pharmacology · 2021Article
- Electrophysiological Properties of Endogenous Single CaInternational journal of molecular sciences · 2021Article
- The Prognostic Value and Mechanisms of TMEM16A in Human Cancer.Frontiers in molecular biosciences · 2021Review
- Notch enhances CaAmerican journal of physiology. Cell physiology · 2020Article
- STIM2 (Stromal Interaction Molecule 2)-Mediated Increase in Resting Cytosolic Free CaHypertension (Dallas, Tex. : 1979) · 2018Article
- Altered expression of PPAR‑γ and TRPC in neonatal rats with persistent pulmonary hypertension.Molecular medicine reports · 2017Article
- Inhibition of phosphodiesterase-5 suppresses calcineurin/NFAT- mediated TRPC6 expression in pulmonary artery smooth muscle cells.Scientific reports · 2017Article
- Notch activation of CaHypertension research : official journal of the Japanese Society of Hypertension · 2017Article
- Pathogenic role of calcium-sensing receptors in the development and progression of pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Modulating Ca²⁺ signals: a common theme for TMEM16, Ist2, and TMC.Pflugers Archiv : European journal of physiology · 2016Review
- ATP promotes cell survival via regulation of cytosolic [Ca2+] and Bcl-2/Bax ratio in lung cancer cells.American journal of physiology. Cell physiology · 2016Article
- Molecular and functional significance of Ca(2+)-activated Cl(-) channels in pulmonary arterial smooth muscle.Pulmonary circulation · 2015Review
- Inhibition of Excessive Cell Proliferation by Calcilytics in Idiopathic Pulmonary Arterial Hypertension.PloS one · 2015Article
- Activation of Notch signaling by short-term treatment with Jagged-1 enhances store-operated Ca(2+) entry in human pulmonary arterial smooth muscle cells.American journal of physiology. Cell physiology · 2014Article
- Inhibition of the Ca(2+)-sensing receptor rescues pulmonary hypertension in rats and mice.Hypertension research : official journal of the Japanese Society of Hypertension · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Intracellular Ca(2+) plays a fundamental role in regulating cell functions in pulmonary arterial smooth muscle cells (PASMCs). A rise in cytosolic Ca(2+) concentration ([Ca(2+)](cyt)) triggers pulmonary vasoconstriction and stimulates PASMC proliferation. [Ca(2+)](cyt) is increased mainly by Ca(2+) release from intracellular stores and Ca(2+) influx through plasmalemmal Ca(2+)-permeable channels. Given the high concentration of intracellular Cl(-) in PASMCs, Ca(2+)-activated Cl(-)(Cl(Ca)) channels play an important role in regulating membrane potential and cell excitability of PASMCs. In this study, we examined whether activity of Cl(Ca) channels was involved in regulating [Ca(2+)](cyt) in human PASMCs via regulating receptor- (ROCE) and store- (SOCE) operated Ca(2+) entry. The data demonstrated that an angiotensin II (100 nM)-mediated increase in [Ca(2+)](cyt) via ROCE was markedly attenuated by the Cl(Ca) channel inhibitors, niflumic acid (100 μM), flufenamic acid (100 μM), and 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (100 μM). The inhibition of Cl(Ca) channels by niflumic acid and flufenamic acid significantly reduced both transient and plateau phases of SOCE that was induced by passive depletion of Ca(2+) from the sarcoplasmic reticulum by 10 μM cyclopiazonic acid. In addition, ROCE and SOCE were abolished by SKF-96365 (50 μM) and 2-aminoethyl diphenylborinate (100 μM), and were slightly decreased in the presence of diltiazem (10 μM). The electrophysiological and immunocytochemical data indicate that Cl(Ca) currents were present and TMEM16A was functionally expressed in human PASMCs. The results from this study suggest that the function of Cl(Ca) channels, potentially formed by TMEM16A proteins, contributes to regulating [Ca(2+)](cyt) by affecting ROCE and SOCE in human PASMCs.
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