ArticlePloS one2012
Increased CD39 nucleotidase activity on microparticles from patients with idiopathic pulmonary arterial hypertension.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 48 citations in OpenAlex.
- Purinergic regulation of pulmonary vascular tone.Purinergic signalling · 2024Review
- Extracellular Purine Metabolism-Potential Target in Multiple Sclerosis.Molecular neurobiology · 2024Review
- Extracellular vesicles in venous thromboembolism and pulmonary hypertension.Journal of nanobiotechnology · 2023Review
- Review
- Circulating Ectonucleotidases Signal Impaired Myocardial Perfusion at Rest and Stress.Journal of the American Heart Association · 2023Article
- CD39 in the development and progression of pulmonary arterial hypertension.Purinergic signalling · 2022Review
- A systematic review with meta-analysis of biomarkers for detection of pulmonary arterial hypertension.ERJ open research · 2022Review
- High levels of extracellular ATP lead to different inflammatory responses in COVID-19 patients according to the severity.Journal of molecular medicine (Berlin, Germany) · 2022Article
- Novel possibility for cutaneous melanoma treatment by means of rosmarinic acid action on purinergic signaling.Purinergic signalling · 2022Review
- Thrombo-Inflammation: A Focus on NTPDase1/CD39.Cells · 2021Review
- Diabetes and hypertension: Pivotal involvement of purinergic signaling.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- Purinergic Dysfunction in Pulmonary Arterial Hypertension.Journal of the American Heart Association · 2020Review
- P2 Purinergic Signaling in the Distal Lung in Health and Disease.International journal of molecular sciences · 2020Review
- Extracellular vesicles: novel communicators in lung diseases.Respiratory research · 2020Review
- Host CD39 Deficiency Affects Radiation-Induced Tumor Growth Delay and Aggravates Radiation-Induced Normal Tissue Toxicity.Frontiers in oncology · 2020Article
- CD73 Promotes Age-Dependent Accretion of Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- CD39 AS A CRITICAL ECTONUCLEOTIDASE DEFENSE AGAINST PATHOLOGICAL VASCULAR REMODELING.Transactions of the American Clinical and Climatological Association · 2018Article
- The Impact of Purinergic System Enzymes on Noncommunicable, Neurological, and Degenerative Diseases.Journal of immunology research · 2018Review
- Cell-derived microparticles and the lung.European respiratory review : an official journal of the European Respiratory Society · 2016Review
- Role of the CD39/CD73 Purinergic Pathway in Modulating Arterial Thrombosis in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundIdiopathic pulmonary arterial hypertension (IPAH) is a devastating disease characterized by increased pulmonary vascular resistance, smooth muscle and endothelial cell proliferation, perivascular inflammatory infiltrates, and in situ thrombosis. Circulating intravascular ATP, ADP, AMP and adenosine activate purinergic cell signaling pathways and appear to induce many of the same pathologic processes that underlie IPAH. Extracellular dephosphorylation of ATP to ADP and AMP occurs primarily via CD39 (ENTPD1), an ectonucleotidase found on the surface of leukocytes, platelets, and endothelial cells. Microparticles are micron-sized phospholipid vesicles formed from the membranes of platelets and endothelial cells.
objectivesStudies here examine whether CD39 is an important microparticle surface nucleotidase, and whether patients with IPAH have altered microparticle-bound CD39 activity that may contribute to the pathophysiology of the disease. METHODOLOGY/PRINCIPAL
findingsKinetic parameters, inhibitor blocking experiments, and immunogold labeling with electron microscopy support the role of CD39 as a major nucleotidase on the surface of microparticles. Comparison of microparticle surface CD39 expression and nucleotidase activity in 10 patients with advanced IPAH and 10 healthy controls using flow cytometry and thin layer chromatograph demonstrate the following: 1) circulating platelet (CD39(+)CD31(+)CD42b(+)) and endothelial (CD39(+)CD31(+)CD42b(-)) microparticle subpopulations in patients with IPAH show increased CD39 expression; 2) microparticle ATPase and ADPase activity in patients with IPAH is increased. CONCLUSIONS/SIGNIFICANCE: We demonstrate for the first time increased CD39 expression and function on circulating microparticles in patients with IPAH. Further research is needed to elucidate whether these findings identify an important trigger for the development of the disease, or reflect a physiologic response to IPAH.
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