ArticleMolecular biology of the cell2018
Neutrophils as sources of dinucleotide polyphosphates and metabolism by epithelial ENPP1 to influence barrier function via adenosine signaling.
Article in Molecular biology of the cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 18 citations in OpenAlex.
- Early alveolar molecular signatures after cardiopulmonary resuscitation: a bronchoalveolar lavage (BALF) proteomic study in swine.Resuscitation plus · 2026Article
- Impact of Neutrophils on the Tissue Microenvironment During Intestinal Inflammation.Journal of inflammation research · 2026Review
- GM-CSF ameliorates inflammation from Pseudomonas aeruginosa in a juvenile mouse model of burn injury.Journal of leukocyte biology · 2025Article
- Chlorination of epithelial tight junction proteins by neutrophil myeloperoxidase promotes barrier dysfunction and mucosal inflammation.JCI insight · 2024Article
- Ecto-5'-nucleotidase (CD73): an emerging role as prognostic factor in allergic sensitization.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- The hypoxic tissue microenvironment as a driver of mucosal inflammatory resolution.Frontiers in immunology · 2023Review
- Hypoxia-inducible factor as a bridge between healthy barrier function, wound healing, and fibrosis.American journal of physiology. Cell physiology · 2022Review
- Metabolic Host-Microbiota Interactions in Autophagy and the Pathogenesis of Inflammatory Bowel Disease (IBD).Pharmaceuticals (Basel, Switzerland) · 2021Review
- Mucosal acidosis elicits a unique molecular signature in epithelia and intestinal tissue mediated by GPR31-induced CREB phosphorylation.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Lung neutrophils on a paleo diet: lean, mean inflammatory machines.The Journal of clinical investigation · 2021Article
- Microbial-derived indoles inhibit neutrophil myeloperoxidase to diminish bystander tissue damage.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Extracellular cyclic dinucleotides induce polarized responses in barrier epithelial cells by adenosine signaling.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Creatine Transporter, Reduced in Colon Tissues From Patients With Inflammatory Bowel Diseases, Regulates Energy Balance in Intestinal Epithelial Cells, Epithelial Integrity, and Barrier Function.Gastroenterology · 2020Article
- Blocking Connexin-43 mediated hemichannel activity protects against early tubular injury in experimental chronic kidney disease.Cell communication and signaling : CCS · 2020Article
- Adaptation to inflammatory acidity through neutrophil-derived adenosine regulation of SLC26A3.Mucosal immunology · 2020Article
- Innate immune cell-epithelial crosstalk during wound repair.The Journal of clinical investigation · 2019Review
- Hypoxia and the regulation of myeloid cell metabolic imprinting: consequences for the inflammatory response.EMBO reports · 2019Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Extracellular adenosine signaling is established as a protective component in mucosal inflammatory responses. The sources of extracellular adenosine include enzymatic processing from nucleotides, such as ATP and AMP, that can be liberated from a variety of cell types, including infiltrating leukocytes. Here we demonstrate that activated human neutrophils are a source of diadenosine triphosphate (Ap3A), providing an additional source of nucleotides during inflammation. Profiling murine enteroids and intestinal epithelial cell lines revealed that intestinal epithelia prominently express apical and lateral ectonucleotide pyrophosphatase/phosphodiesterase-1 (ENPP1), a member of the ENPP family of enzymes that metabolize diadenosine phosphates, especially Ap3A. Extensions of these studies demonstrated that intestinal epithelia metabolize Ap3A to ADP and AMP, which are further metabolized to adenosine and made available to activate surface adenosine receptors. Using loss and gain of ENPP1 approaches, we revealed that ENPP1 coordinates epithelial barrier formation and promotes epithelial wound healing responses. These studies demonstrate the cooperative metabolism between Ap3A and ENPP1 function to provide a significant source of adenosine, subserving its role in inflammatory resolution.
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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.