ArticleArteriosclerosis, thrombosis, and vascular biology2019
Tuning the Thromboinflammatory Response to Venous Flow Interruption by the Ectonucleotidase CD39.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
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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
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Effects of physical exercise on the functionality of human nucleotidases: A systematic review.Physiological reports · 2022Pooled it
- A Coordinated Translational Control Mediated by eEF2 Phosphorylation Safeguards Erythroid Differentiation.International journal of molecular sciences · 2025Article
- Extracellular purines in lung endothelial permeability and pulmonary diseases.Frontiers in physiology · 2024Review
- Causality of genetically proxied immunophenotypes on cardiovascular diseases: a Mendelian randomization study.Frontiers in immunology · 2024Article
- Inflammasome Signaling, Thromboinflammation, and Venous Thromboembolism.JACC. Basic to translational science · 2023Review
- Poststroke venous thromboembolism and neutrophil activation: an illustrated review.Research and practice in thrombosis and haemostasis · 2023Article
- Purinergic signaling: a potential therapeutic target for ischemic stroke.Purinergic signalling · 2023Review
- Platelet-Neutrophil Interaction and Thromboinflammation in Diabetes: Considerations for Novel Therapeutic Approaches.Journal of the American Heart Association · 2022Review
- Endothelial Cell Phenotype, a Major Determinant of Venous Thrombo-Inflammation.Frontiers in cardiovascular medicine · 2022Review
- Thrombo-Inflammation: A Focus on NTPDase1/CD39.Cells · 2021Review
- Inflammation, Infection and Venous Thromboembolism.Circulation research · 2021Review
- Gab2 (Grb2-Associated Binder2) Plays a Crucial Role in Inflammatory Signaling and Endothelial Dysfunction.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- New (re)purpose for an old drug: purinergic modulation may extinguish the COVID-19 thromboinflammatory firestorm.JCI insight · 2020Article
- Recent Insights Into the Regulation of Coagulation and Thrombosis.Arteriosclerosis, thrombosis, and vascular biology · 2020Review
- Ectonucleoside Triphosphate Diphosphohydrolase-1/CD39 Affects the Response to ADP of Female Rat Platelets.Frontiers in pharmacology · 2019Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
Objective- Leukocyte flux contributes to thrombus formation in deep veins under pathological conditions, but mechanisms that inhibit venous thrombosis are incompletely understood. Ectonucleotide di(tri)phosphohydrolase 1 ( ENTPD1 or Cd39), an ectoenzyme that catabolizes extracellular adenine nucleotides, is embedded on the surface of endothelial cells and leukocytes. We hypothesized that under venous stasis conditions, CD39 regulates inflammation at the vein:blood interface in a murine model of deep vein thrombosis. Approach and Results- CD39-null mice developed significantly larger venous thrombi under venous stasis, with more leukocyte recruitment compared with wild-type mice. Gene expression profiling of wild-type and Cd39-null mice revealed 76 differentially expressed inflammatory genes that were significantly upregulated in Cd39-deleted mice after venous thrombosis, and validation experiments confirmed high expression of several key inflammatory mediators. P-selectin, known to have proximal involvement in venous inflammatory and thrombotic events, was upregulated in Cd39-null mice. Inferior vena caval ligation resulted in thrombosis and a corresponding increase in both P-selectin and VWF (von Willebrand Factor) levels which were strikingly higher in mice lacking the Cd39 gene. These mice also manifest an increase in circulating platelet-leukocyte heteroaggregates suggesting heterotypic crosstalk between coagulation and inflammatory systems, which is amplified in the absence of CD39. Conclusions- These data suggest that CD39 mitigates the venous thromboinflammatory response to flow interruption.
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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.