ArticleBlood2017
Circulating soluble P-selectin must dimerize to promote inflammation and coagulation in mice.
Article in Blood, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 98 citations in OpenAlex.
- Targeting protein disulfide isomerase with the flavonoid isoquercetin to improve hypercoagulability in advanced cancer.JCI insight · 2019Trial
- P-Selectin Level at First and Third Day After Portal Hypertensive Splenectomy for Early Prediction of Portal Vein Thrombosis in Patients With Cirrhosis.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis · 2018Trial
- Inflammatory and Cardiovascular Responses to Active and Passive Acute Psychological Stress.Biopsychosocial science and medicineTrial
- NET-mediated immunothrombosis in ischemic stroke: pathobiology, biomarkers, and therapeutic targeting.Thrombosis journal · 2026Review
- Elevated neuraminidase potentiates lung inflammation through facilitating integrin β2-mediated adhesion and immune responses of neutrophils.The Journal of biological chemistry · 2026Article
- Neutrophil death pathways in myocardial infarction: the balance between injury and repair.Frontiers in immunology · 2026Review
- Impact of Preanalytical Storage Time and Air Exposure on ROTEM and Coagulation Sample Stability.Advances in hematology · 2026Article
- Neutrophils Induce P-Selectin Shedding from Activated Platelets Via Neutrophil Elastase.Inflammation · 2025Article
- Platelet activation plays a pro-inflammatory role in myasthenia gravis.Nature communications · 2025Article
- Precision Medicine for Diabetic Retinopathy: Integrating Genetics, Biomarkers, Lifestyle, and AI.Genes · 2025Review
- Dysregulation of immune cells and platelet-monocyte aggregates in chronic thromboembolic pulmonary hypertension.Respiratory research · 2025Article
- Review
- Physiological significance of antithrombin D-helix interaction with vascular GAGs.Blood advances · 2025Article
- Sialyl LewisACS medicinal chemistry letters · 2025Article
- Platelets in infection: intrinsic roles and functional outcomes.Frontiers in immunology · 2025Review
- Rapid prediction of acute thrombosis via nanoengineered immunosensors with unsupervised clustering for multiple circulating biomarkers.Science advances · 2024Article
- Proteomic profiling for biomarker discovery in heparin-induced thrombocytopenia.Blood advances · 2024Article
- Microvesicles from stored red blood cells induce P-selectin and von Willebrand factor release from endothelial cells via a protein kinase C-dependent mechanism.Transfusion and apheresis science : official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis · 2024Article
- Viral uptake and pathophysiology of the lung endothelial cells in age-associated severe SARS-CoV-2 infection models.Aging cell · 2024Article
- Exploration on the effect of anserine on the alleviation of DVT and its molecular mechanism.Frontiers in pharmacology · 2024Article
Corrections and comments
- Commented on by
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Leukocyte adhesion to P-selectin on activated platelets and endothelial cells induces shedding of the P-selectin ectodomain into the circulation. Plasma soluble P-selectin (sP-selectin) is elevated threefold to fourfold in patients with cardiovascular disease. Circulating sP-selectin is thought to trigger signaling in leukocytes that directly contributes to inflammation and thrombosis. However, sP-selectin likely circulates as a monomer, and in vitro studies suggest that sP-selectin must dimerize to induce signaling in leukocytes. To address this discrepancy, we expressed the entire ectodomain of mouse P-selectin as a monomer (sP-selectin) or as a disulfide-linked dimer fused to the Fc portion of mouse immunoglobulin G (sP-selectin-Fc). Dimeric sP-selectin-Fc, but not monomeric sP-selectin, triggered integrin-dependent adhesion of mouse leukocytes in vitro. Antibody-induced oligomerization of sP-selectin or sP-selectin-Fc was required to trigger formation of neutrophil extracellular traps. Injecting sP-selectin-Fc, but not sP-selectin, into mice augmented integrin-dependent adhesion of neutrophils in venules, generated tissue factor-bearing microparticles, shortened plasma-clotting times, and increased thrombus frequency in the inferior vena cava. Furthermore, transgenic mice that overexpressed monomeric sP-selectin did not exhibit increased inflammation or thrombosis. We conclude that elevated plasma sP-selectin is a consequence rather than a cause of cardiovascular disease.
Indexed as
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.