ArticlePurinergic signalling2006
E-NTPDases in human airways: Regulation and relevance for chronic lung diseases.
Article in Purinergic signalling, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
The trial behind it
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
16 citing papers in PubMed, 36 citations in OpenAlex.
- Purinergic regulation of pulmonary vascular tone.Purinergic signalling · 2024Review
- Epithelial miR-206 targets CD39/extracellular ATP to upregulate airway IL-25 and TSLP in type 2-high asthma.JCI insight · 2021Article
- Purinergic receptors in airway hydration.Biochemical pharmacology · 2021Review
- Ectonucleotidases in Inflammation, Immunity, and Cancer.Journal of immunology (Baltimore, Md. : 1950) · 2021Review
- The therapeutic potential of inorganic polyphosphate: A versatile physiological polymer to control coronavirus disease (COVID-19).Theranostics · 2021Review
- Inhibition of ATP hydrolysis restores airway surface liquid production in cystic fibrosis airway epithelia.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Is the purinergic pathway involved in the pathology of COPD? Decreased lung CD39 expression at initial stages of COPD.Respiratory research · 2018Observational
- The ectonucleotidases CD39 and CD73: Novel checkpoint inhibitor targets.Immunological reviews · 2017Review
- Protective effect of quercetin in ecto-enzymes, cholinesterases, and myeloperoxidase activities in the lymphocytes of rats exposed to cadmium.Molecular and cellular biochemistry · 2014Article
- CD39 is a negative regulator of P2X7-mediated inflammatory cell death in mast cells.Cell communication and signaling : CCS · 2014Article
- Article
- Cellular function and molecular structure of ecto-nucleotidases.Purinergic signalling · 2012Review
- Cystic fibrosis remodels the regulation of purinergic signaling by NTPDase1 (CD39) and NTPDase3.American journal of physiology. Lung cellular and molecular physiology · 2010Article
- Mathematical model of nucleotide regulation on airway epithelia. Implications for airway homeostasis.The Journal of biological chemistry · 2008Article
- Physiological regulation of ATP release at the apical surface of human airway epithelia.The Journal of biological chemistry · 2006Article
- The E-NTPDase family of ectonucleotidases: Structure function relationships and pathophysiological significance.Purinergic signalling · 2006Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic obstructive lung diseases are characterized by the inability to prevent bacterial infection and a gradual loss of lung function caused by recurrent inflammatory responses. In the past decade, numerous studies have demonstrated the importance of nucleotide-mediated bacterial clearance. Their interaction with P2 receptors on airway epithelia provides a rapid 'on-and-off' signal stimulating mucus secretion, cilia beating activity and surface hydration. On the other hand, abnormally high ATP levels resulting from damaged epithelia and bacterial lysis may cause lung edema and exacerbate inflammatory responses. Airway ATP concentrations are regulated by ecto nucleoside triphosphate diphosphohydrolases (E-NTPDases) which are expressed on the mucosal surface and catalyze the sequential dephosphorylation of nucleoside triphosphates to nucleoside monophosphates (ATP --> ADP --> AMP). The common bacterial product, Pseudomonas aeruginosa lipopolysaccharide (LPS), induces an acute reduction in azide-sensitive E-NTPDase activities, followed by a sustained increase in activity as well as NTPDase 1 and NTPDase 3 expression. Accordingly, chronic lung diseases, including cystic fibrosis (CF) and primary ciliary dyskinesia, are characterized by higher rates of nucleotide elimination, azide-sensitive E-NTPDase activities and expression. This review integrates the biphasic regulation of airway E-NTPDases with the function of purine signaling in lung diseases. During acute insults, a transient reduction in E-NTPDase activities may be beneficial to stimulate ATP-mediated bacterial clearance. In chronic lung diseases, elevating E-NTPDase activities may represent an attempt to prevent P2 receptor desensitization and nucleotide-mediated lung damage.
Identifiers
What OpenQuestion holds
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.