ArticleArteriosclerosis, thrombosis, and vascular biology2016
Role of the CD39/CD73 Purinergic Pathway in Modulating Arterial Thrombosis in Mice.
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Article in Arteriosclerosis, thrombosis, and vascular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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30citing papers in PubMed
3.8field-weighted citation impact, top 8% of its field
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Who cites it
30 citing papers in PubMed, 42 citations in OpenAlex.
- Comparison of the expression of cluster of differentiation (CD)39 and CD73 between propofol- and sevoflurane-based anaesthesia during open heart surgery.Scientific reports · 2018Trial
- From danger to resolution: targeting purinergic signaling in CNS diseases.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Review
- Pathogenic role of serpin B3-positive neutrophils in reinforcing thrombus stiffening during ischemic stroke.Blood · 2026Article
- The myofascial rheostat: hyaluronan molecular weight dynamics and purinergic signalling as a physiological feedback system.Frontiers in physiology · 2026Review
- The CD39-CD73-adenosine axis: a pivotal regulator of retinal homeostasis and diseases.Frontiers in cell and developmental biology · 2026Review
- Targeted knock-in of human immune-regulatory genes into the porcine GGTA1 exon 4 reveals divergent expression on red blood cell membranes.Scientific reports · 2025Article
- Article
- Causality of genetically proxied immunophenotypes on cardiovascular diseases: a Mendelian randomization study.Frontiers in immunology · 2024Article
- Extracellular purines in lung endothelial permeability and pulmonary diseases.Frontiers in physiology · 2024Review
- The role of CD38 in ischemia reperfusion injury in cardiopulmonary bypass and thoracic transplantation: a narrative review.Journal of thoracic disease · 2023Review
- Purinergic signaling: a potential therapeutic target for ischemic stroke.Purinergic signalling · 2023Review
- Ectonucleoside triphosphate diphosphohydrolase-1 (CD39) impacts TGF-β1 responses: insights into cardiac fibrosis and function following myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2022Article
- Effects of human TFPI and CD47 expression and selectin and integrin inhibition during GalTKO.hCD46 pig lung perfusion with human blood.Xenotransplantation · 2022Article
- A Recombinant Fusion Construct between Human Serum Albumin and NTPDase CD39 Allows Anti-Inflammatory and Anti-Thrombotic Coating of Medical Devices.Pharmaceutics · 2021Article
- The Adenosine Pathway and Human Immunodeficiency Virus-Associated Inflammation.Open forum infectious diseases · 2021Review
- Purinergic Signalling in Allogeneic Haematopoietic Stem Cell Transplantation and Graft-versus-Host Disease.International journal of molecular sciences · 2021Review
- Possible role of purinergic signaling in COVID-19.Molecular and cellular biochemistry · 2021Review
- Role of Purinergic Signalling in Endothelial Dysfunction and Thrombo-Inflammation in Ischaemic Stroke and Cerebral Small Vessel Disease.Biomolecules · 2021Review
- Expression and Gene Regulation Network of Adenosine Receptor A2B in Lung Adenocarcinoma: A Potential Diagnostic and Prognostic Biomarker.Frontiers in molecular biosciences · 2021Article
- De novo transcriptome sequencing of Paecilomyces tenuipes revealed genes involved in adenosine biosynthesis.Molecular medicine reports · 2020Article
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Authors and funding
12 authors at 4 institutions in 2 countries.
Roman CovarrubiasFrom the Division of Cardiovascular Medicine, Department of Medicine (R.C., E.C., T.N., R.J.G.), Department of Pharmacology (R.J.G.), and Department of Pathology Microbiology and Immunology (R.J.G.), Vanderbilt University, Nashville, TN; Division of Cardiovascular Medicine, Davis Heart and Lung Research Institute, The Ohio State University, Columbus (A.R., Z.M.H., R.H., K.S., D.G.W.); Transplant Institute, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA (S.C.R.); School of Medicine, Deakin University (K.M.D., P.J.C.); Immunology Research Centre, St. Vincent's Hospital (K.M.D.); and Department of Medicine, University of Melbourne, Victoria, Australia (K.M.D., P.J.C.).
Elena ChepurkoFrom the Division of Cardiovascular Medicine, Department of Medicine (R.C., E.C., T.N., R.J.G.), Department of Pharmacology (R.J.G.), and Department of Pathology Microbiology and Immunology (R.J.G.), Vanderbilt University, Nashville, TN; Division of Cardiovascular Medicine, Davis Heart and Lung Research Institute, The Ohio State University, Columbus (A.R., Z.M.H., R.H., K.S., D.G.W.); Transplant Institute, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA (S.C.R.); School of Medicine, Deakin University (K.M.D., P.J.C.); Immunology Research Centre, St. Vincent's Hospital (K.M.D.); and Department of Medicine, University of Melbourne, Victoria, Australia (K.M.D., P.J.C.).
Adam ReynoldsFrom the Division of Cardiovascular Medicine, Department of Medicine (R.C., E.C., T.N., R.J.G.), Department of Pharmacology (R.J.G.), and Department of Pathology Microbiology and Immunology (R.J.G.), Vanderbilt University, Nashville, TN; Division of Cardiovascular Medicine, Davis Heart and Lung Research Institute, The Ohio State University, Columbus (A.R., Z.M.H., R.H., K.S., D.G.W.); Transplant Institute, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA (S.C.R.); School of Medicine, Deakin University (K.M.D., P.J.C.); Immunology Research Centre, St. Vincent's Hospital (K.M.D.); and Department of Medicine, University of Melbourne, Victoria, Australia (K.M.D., P.J.C.).
Zachary M HuttingerFrom the Division of Cardiovascular Medicine, Department of Medicine (R.C., E.C., T.N., R.J.G.), Department of Pharmacology (R.J.G.), and Department of Pathology Microbiology and Immunology (R.J.G.), Vanderbilt University, Nashville, TN; Division of Cardiovascular Medicine, Davis Heart and Lung Research Institute, The Ohio State University, Columbus (A.R., Z.M.H., R.H., K.S., D.G.W.); Transplant Institute, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA (S.C.R.); School of Medicine, Deakin University (K.M.D., P.J.C.); Immunology Research Centre, St. Vincent's Hospital (K.M.D.); and Department of Medicine, University of Melbourne, Victoria, Australia (K.M.D., P.J.C.).
Ryan HuttingerFrom the Division of Cardiovascular Medicine, Department of Medicine (R.C., E.C., T.N., R.J.G.), Department of Pharmacology (R.J.G.), and Department of Pathology Microbiology and Immunology (R.J.G.), Vanderbilt University, Nashville, TN; Division of Cardiovascular Medicine, Davis Heart and Lung Research Institute, The Ohio State University, Columbus (A.R., Z.M.H., R.H., K.S., D.G.W.); Transplant Institute, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA (S.C.R.); School of Medicine, Deakin University (K.M.D., P.J.C.); Immunology Research Centre, St. Vincent's Hospital (K.M.D.); and Department of Medicine, University of Melbourne, Victoria, Australia (K.M.D., P.J.C.).
Katherine StanfillFrom the Division of Cardiovascular Medicine, Department of Medicine (R.C., E.C., T.N., R.J.G.), Department of Pharmacology (R.J.G.), and Department of Pathology Microbiology and Immunology (R.J.G.), Vanderbilt University, Nashville, TN; Division of Cardiovascular Medicine, Davis Heart and Lung Research Institute, The Ohio State University, Columbus (A.R., Z.M.H., R.H., K.S., D.G.W.); Transplant Institute, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA (S.C.R.); School of Medicine, Deakin University (K.M.D., P.J.C.); Immunology Research Centre, St. Vincent's Hospital (K.M.D.); and Department of Medicine, University of Melbourne, Victoria, Australia (K.M.D., P.J.C.).
Debra G WheelerFrom the Division of Cardiovascular Medicine, Department of Medicine (R.C., E.C., T.N., R.J.G.), Department of Pharmacology (R.J.G.), and Department of Pathology Microbiology and Immunology (R.J.G.), Vanderbilt University, Nashville, TN; Division of Cardiovascular Medicine, Davis Heart and Lung Research Institute, The Ohio State University, Columbus (A.R., Z.M.H., R.H., K.S., D.G.W.); Transplant Institute, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA (S.C.R.); School of Medicine, Deakin University (K.M.D., P.J.C.); Immunology Research Centre, St. Vincent's Hospital (K.M.D.); and Department of Medicine, University of Melbourne, Victoria, Australia (K.M.D., P.J.C.).
Tatiana NovitskayaFrom the Division of Cardiovascular Medicine, Department of Medicine (R.C., E.C., T.N., R.J.G.), Department of Pharmacology (R.J.G.), and Department of Pathology Microbiology and Immunology (R.J.G.), Vanderbilt University, Nashville, TN; Division of Cardiovascular Medicine, Davis Heart and Lung Research Institute, The Ohio State University, Columbus (A.R., Z.M.H., R.H., K.S., D.G.W.); Transplant Institute, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA (S.C.R.); School of Medicine, Deakin University (K.M.D., P.J.C.); Immunology Research Centre, St. Vincent's Hospital (K.M.D.); and Department of Medicine, University of Melbourne, Victoria, Australia (K.M.D., P.J.C.).
Simon C RobsonFrom the Division of Cardiovascular Medicine, Department of Medicine (R.C., E.C., T.N., R.J.G.), Department of Pharmacology (R.J.G.), and Department of Pathology Microbiology and Immunology (R.J.G.), Vanderbilt University, Nashville, TN; Division of Cardiovascular Medicine, Davis Heart and Lung Research Institute, The Ohio State University, Columbus (A.R., Z.M.H., R.H., K.S., D.G.W.); Transplant Institute, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA (S.C.R.); School of Medicine, Deakin University (K.M.D., P.J.C.); Immunology Research Centre, St. Vincent's Hospital (K.M.D.); and Department of Medicine, University of Melbourne, Victoria, Australia (K.M.D., P.J.C.).
Karen M DwyerFrom the Division of Cardiovascular Medicine, Department of Medicine (R.C., E.C., T.N., R.J.G.), Department of Pharmacology (R.J.G.), and Department of Pathology Microbiology and Immunology (R.J.G.), Vanderbilt University, Nashville, TN; Division of Cardiovascular Medicine, Davis Heart and Lung Research Institute, The Ohio State University, Columbus (A.R., Z.M.H., R.H., K.S., D.G.W.); Transplant Institute, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA (S.C.R.); School of Medicine, Deakin University (K.M.D., P.J.C.); Immunology Research Centre, St. Vincent's Hospital (K.M.D.); and Department of Medicine, University of Melbourne, Victoria, Australia (K.M.D., P.J.C.).
Peter J CowanFrom the Division of Cardiovascular Medicine, Department of Medicine (R.C., E.C., T.N., R.J.G.), Department of Pharmacology (R.J.G.), and Department of Pathology Microbiology and Immunology (R.J.G.), Vanderbilt University, Nashville, TN; Division of Cardiovascular Medicine, Davis Heart and Lung Research Institute, The Ohio State University, Columbus (A.R., Z.M.H., R.H., K.S., D.G.W.); Transplant Institute, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA (S.C.R.); School of Medicine, Deakin University (K.M.D., P.J.C.); Immunology Research Centre, St. Vincent's Hospital (K.M.D.); and Department of Medicine, University of Melbourne, Victoria, Australia (K.M.D., P.J.C.).
Richard J GuminaFrom the Division of Cardiovascular Medicine, Department of Medicine (R.C., E.C., T.N., R.J.G.), Department of Pharmacology (R.J.G.), and Department of Pathology Microbiology and Immunology (R.J.G.), Vanderbilt University, Nashville, TN; Division of Cardiovascular Medicine, Davis Heart and Lung Research Institute, The Ohio State University, Columbus (A.R., Z.M.H., R.H., K.S., D.G.W.); Transplant Institute, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA (S.C.R.); School of Medicine, Deakin University (K.M.D., P.J.C.); Immunology Research Centre, St. Vincent's Hospital (K.M.D.); and Department of Medicine, University of Melbourne, Victoria, Australia (K.M.D., P.J.C.). richard.gumina@vanderbilt.edu.
Beth Israel Deaconess Medical Center · USVanderbilt University · USDeakin University · AUSt Vincent's Hospital · AU
Funding
Training In Cardiovascular ResearchT32HL007411 · NHLBI · VANDERBILT UNIVERSITY · PI BECKMAN, JOSHUA A · 1985 to 2020
$7.2MVanderbilt Student Research Training ProgramT35DK007383 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI William Heerman · 1986 to 2026
$4.1MPurinergic ThromboregulationR01HL094400 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROBSON, SIMON C. · 2009 to 2010
$1.4MEffect of sarcolemmal KATP channels on ROS/RNS generation and calcium handlingK08HL094703 · NHLBI · VANDERBILT UNIVERSITY · PI GUMINA, RICHARD J · 2009 to 2013
$600kCD39-mediated cardiovascular protectionR21HL096038 · NHLBI · OHIO STATE UNIVERSITY · PI GUMINA, RICHARD J · 2009 to 2010
$413kNHLBI NIH HHS K08 HL094703NHLBI NIH HHS R01 HL094400NHLBI NIH HHS R21 HL096038NHLBI NIH HHS T32 HL007411NIDDK NIH HHS T35 DK007383
Abstract
objectiveCirculating blood cells and endothelial cells express ectonucleoside triphosphate diphosphohydrolase-1 (CD39) and ecto-5'-nucleotidase (CD73). CD39 hydrolyzes extracellular ATP or ADP to AMP. CD73 hydrolyzes AMP to adenosine. The goal of this study was to examine the interplay between CD39 and CD73 cascade in arterial thrombosis. APPROACH AND
resultsTo determine how CD73 activity influences in vivo thrombosis, the time to ferric chloride-induced arterial thrombosis was measured in CD73-null mice. In response to 5% FeCl3, but not to 10% FeCl3, there was a significant decrease in the time to thrombosis in CD73-null mice compared with wild-type mice. In mice overexpressing CD39, ablation of CD73 did not inhibit the prolongation in the time to thrombosis conveyed by CD39 overexpression. However, the CD73 inhibitor α-β-methylene-ADP nullified the prolongation in the time to thrombosis in human CD39 transgenic (hC39-Tg)/CD73-null mice. To determine whether hematopoietic-derived cells or endothelial cell CD39 activity regulates in vivo arterial thrombus, bone marrow transplant studies were conducted. FeCl3-induced arterial thrombosis in chimeric mice revealed a significant prolongation in the time to thrombosis in hCD39-Tg reconstituted wild-type mice, but not on wild-type reconstituted hCD39-Tg mice. Monocyte depletion with clodronate-loaded liposomes normalized the time to thrombosis in hCD39-Tg mice compared with hCD39-Tg mice treated with control liposomes, demonstrating that increased CD39 expression on monocytes protects against thrombosis.
conclusionsThese data demonstrate that ablation of CD73 minimally effects in vivo thrombosis, but increased CD39 expression on hematopoietic-derived cells, especially monocytes, attenuates in vivo arterial thrombosis.
Indexed as
Blood Coagulation5'-NucleotidaseAdenosineAdenosine DiphosphateAdenosine MonophosphateAdenosine TriphosphateAnimalsAntigens, CDApyraseArterial Occlusive DiseasesBone Marrow TransplantationChloridesDisease Models, AnimalEndothelial CellsFerric CompoundsGenetic Predisposition to Disease5'-NucleotidaseAdenosineAdenosine DiphosphateAdenosine MonophosphateAdenosine TriphosphateAntigens, CDApyraseCD39 antigenChloridesferric chlorideFerric Compoundsadenosine diphosphatemonocytesnucleotidaseplatelet activationthrombosis
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