ArticleThe Journal of general physiology2001
Polarized signaling via purinoceptors in normal and cystic fibrosis airway epithelia.
Article in The Journal of general physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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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.
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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
44 citing papers in PubMed, 113 citations in OpenAlex.
- Niclosamide does not modulate airway epithelial function through blocking of the calcium activated chloride channel, TMEM16A.Frontiers in pharmacology · 2023Article
- Extracellular Nucleotides and Histamine Suppress TLR3- and RIG-I-Mediated Release of Antiviral IFNs from Human Airway Epithelial Cells.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- TMEM16A Potentiation: A Novel Therapeutic Approach for the Treatment of Cystic Fibrosis.American journal of respiratory and critical care medicine · 2020Article
- TMEM16A: An Alternative Approach to Restoring Airway Anion Secretion in Cystic Fibrosis?International journal of molecular sciences · 2020Review
- Increases in cytosolic CaCellular and molecular life sciences : CMLS · 2019Article
- Mucin Production and Hydration Responses to Mucopurulent Materials in Normal versus Cystic Fibrosis Airway Epithelia.American journal of respiratory and critical care medicine · 2018Article
- ATP Release from Human Airway Epithelial Cells Exposed to Staphylococcus aureus Alpha-Toxin.Toxins · 2016Article
- Coupling of TRPV6 and TMEM16A in epithelial principal cells of the rat epididymis.The Journal of general physiology · 2016Article
- A spatial model of fluid recycling in the airways of the lung.Journal of theoretical biology · 2015Article
- UTP activates small-conductance Ca2+-activated K+ channels in murine detrusor PDGFRα+ cells.American journal of physiology. Renal physiology · 2015Article
- Abnormal n-6 fatty acid metabolism in cystic fibrosis is caused by activation of AMP-activated protein kinase.Journal of lipid research · 2014Article
- Tgf-beta downregulation of distinct chloride channels in cystic fibrosis-affected epithelia.PloS one · 2014Article
- Article
- CFTR induces extracellular acid sensing in Xenopus oocytes which activates endogenous Ca²⁺-activated Cl⁻ conductance.Pflugers Archiv : European journal of physiology · 2011Article
- Functional apical large conductance, Ca2+-activated, and voltage-dependent K+ channels are required for maintenance of airway surface liquid volume.The Journal of biological chemistry · 2011Article
- Suppression of CFTR-mediated Cl secretion of airway epithelium in vitamin C-deficient mice.Journal of Korean medical science · 2011Article
- Identification and functional characterization of TMEM16A, a Ca2+-activated Cl- channel activated by extracellular nucleotides, in biliary epithelium.The Journal of biological chemistry · 2011Article
- Ion transport regulation by P2Y receptors, protein kinase C and phosphatidylinositol 3-kinase within the semicircular canal duct epithelium.BMC research notes · 2010Article
- Airway epithelial inflammation-induced endoplasmic reticulum Ca2+ store expansion is mediated by X-box binding protein-1.The Journal of biological chemistry · 2009Article
- Role of mechanical stress in regulating airway surface hydration and mucus clearance rates.Respiratory physiology & neurobiology · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Airway epithelia are confronted with distinct signals emanating from the luminal and/or serosal environments. This study tested whether airway epithelia exhibit polarized intracellular free calcium (Ca(2+)(i)) and anion secretory responses to 5' triphosphate nucleotides (ATP/UTP), which may be released across both barriers of these epithelia. In both normal and cystic fibrosis (CF) airway epithelia, mucosal exposure to ATP/UTP increased Ca(2+)(i) and anion secretion, but both responses were greater in magnitude for CF epithelia. In CF epithelia, the mucosal nucleotide-induced response was mediated exclusively via Ca(2+)(i) interacting with a Ca(2+)-activated Cl(-) channel (CaCC). In normal airway epithelia (but not CF), nucleotides stimulated a component of anion secretion via a chelerythrine-sensitive, Ca(2+)-independent PKC activation of cystic fibrosis transmembrane conductance regulator. In normal and CF airway epithelia, serosally applied ATP or UTP were equally effective in mobilizing Ca(2+)(i). However, serosally applied nucleotides failed to induce anion transport in CF epithelia, whereas a PKC-regulated anion secretory response was detected in normal airway epithelia. We conclude that (1) in normal nasal epithelium, apical/basolateral purinergic receptor activation by ATP/UTP regulates separate Ca(2+)-sensitive and Ca(2+)-insensitive (PKC-mediated) anion conductances; (2) in CF airway epithelia, the mucosal ATP/UTP-dependent anion secretory response is mediated exclusively via Ca(2+)(i); and (3) Ca(2+)(i) regulation of the Ca(2+)-sensitive anion conductance (via CaCC) is compartmentalized in both CF and normal airway epithelia, with basolaterally released Ca(2+)(i) failing to activate CaCC in both epithelia.
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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.