ArticleJournal of cellular physiology2015
TRPC1 regulates calcium-activated chloride channels in salivary gland cells.
Article in Journal of cellular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 47 citations in OpenAlex.
- Physiological functions and pharmacological targeting of transient receptor potential channels.Pharmacological reviews · 2025Review
- Discovery of Fungus-Derived Nornidulin as a Novel TMEM16A Inhibitor: A Potential Therapy to Inhibit Mucus Secretion in Asthma.Journal of experimental pharmacology · 2023Article
- Salivary gland function, development, and regeneration.Physiological reviews · 2022Review
- Xanthine Oxidase Inhibitor, Febuxostat Is Effective against 5-Fluorouracil-Induced Parotid Salivary Gland Injury in Rats Via Inhibition of Oxidative Stress, Inflammation and Targeting TRPC1/CHOP Signalling Pathway.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Molecular mechanisms of activation and regulation of ANO1-Encoded CaChannels (Austin, Tex.) · 2021Review
- Chloride channel accessory 1 integrates chloride channel activity and mTORC1 in aging-related kidney injury.Aging cell · 2021Article
- Electrophysiological Properties of Endogenous Single CaInternational journal of molecular sciences · 2021Article
- Function of the PorcineCells · 2021Article
- The Prognostic Value and Mechanisms of TMEM16A in Human Cancer.Frontiers in molecular biosciences · 2021Review
- Epigenetic Modification of CFTR in Head and Neck Cancer.Journal of clinical medicine · 2020Article
- Article
- The Endoplasmic Reticulum-Plasma Membrane Junction: A Hub for Agonist Regulation of CaCold Spring Harbor perspectives in biology · 2020Review
- The multifaceted role of TMEM16A in cancer.Cell calcium · 2019Review
- TMEM16A controls EGF-induced calcium signaling implicated in pancreatic cancer prognosis.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- CRAC channels in secretory epithelial cell function and disease.Cell calcium · 2019Review
- TRPC1 expression and function inhibit ER stress and cell death in salivary gland cells.FASEB bioAdvances · 2019Article
- Ion Channels in Pulmonary Hypertension: A Therapeutic Interest?International journal of molecular sciences · 2018Review
- Review
- Cell-specific mechanisms of TMEM16A CaMolecular cancer · 2017Review
- TRPC1, Orai1, and STIM1 in SOCE: Friends in tight spaces.Cell calcium · 2017Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Calcium-activated chloride channel (CaCC) plays an important role in modulating epithelial secretion. It has been suggested that in salivary tissues, sustained fluid secretion is dependent on Ca(2+) influx that activates ion channels such as CaCC to initiate Cl(-) efflux. However direct evidence as well as the molecular identity of the Ca(2+) channel responsible for activating CaCC in salivary tissues is not yet identified. Here we provide evidence that in human salivary cells, an outward rectifying Cl(-) current was activated by increasing [Ca(2+)]i, which was inhibited by the addition of pharmacological agents niflumic acid (NFA), an antagonist of CaCC, or T16Ainh-A01, a specific TMEM16a inhibitor. Addition of thapsigargin (Tg), that induces store-depletion and activates TRPC1-mediated Ca(2+) entry, potentiated the Cl(-) current, which was inhibited by the addition of a non-specific TRPC channel blocker SKF96365 or removal of external Ca(2+). Stimulation with Tg also increased plasma membrane expression of TMEM16a protein, which was also dependent on Ca(2+) entry. Importantly, in salivary cells, TRPC1 silencing, but not that of TRPC3, inhibited CaCC especially upon store depletion. Moreover, primary acinar cells isolated from submandibular gland also showed outward rectifying Cl(-) currents upon increasing [Ca(2+)]i. These Cl(-) currents were again potentiated with the addition of Tg, but inhibited in the presence of T16Ainh-A01. Finally, acinar cells isolated from the submandibular glands of TRPC1 knockout mice showed significant inhibition of the outward Cl(-) currents without decreasing TMEM16a expression. Together the data suggests that Ca(2+) entry via the TRPC1 channels is essential for the activation of CaCC.
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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.