ArticleBlood2008
Thrombospondin-1 stimulates platelet aggregation by blocking the antithrombotic activity of nitric oxide/cGMP signaling.
Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 1 of them a synthesis that pooled it.
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.
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
117 citing papers in PubMed, 1 synthesis or guideline pooled it, 197 citations in OpenAlex.
- Pooled it
- Thrombospondin-1 gene polymorphism is associated with estimated pulmonary artery pressure in patients with sickle cell anemia.American journal of hematology · 2017Trial
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- SIRPα ablated iPSC-derived macrophages resist hypophagia and enhance mAb-dependent and CAR-mediated cytotoxicity of solid tumors.Molecular therapy. Oncology · 2026Article
- Present Advances and Emerging Challenges in Kidney Xenotransplantation.Journal of clinical medicine · 2026Review
- Multiparametric assessment of atrial cardiopathy in cryptogenic stroke patients: Implications for personalized clinical management.European stroke journal · 2026Article
- Review
- Multiparametric assessment of atrial cardiopathy in cryptogenic stroke patients: Implications for personalized clinical management.European stroke journal · 2025Article
- The mechanobiology of extracellular matrix: a focus on thrombospondins.Cell communication and signaling : CCS · 2025Review
- Evaluation of thrombospondin 1 as a novel biomarker in pediatric-onset systemic lupus erythematosus.BMC pediatrics · 2025Article
- The Proteome Content of Blood Clots Observed Under Different Conditions: Successful Role in Predicting Clot Amyloid(ogenicity).Molecules (Basel, Switzerland) · 2025Review
- Inflammatory Gene Expression in Livers Undergoing Ex Situ Normothermic Perfusion Is Attenuated by Leukocyte Removal From the Perfusate.Transplantation · 2025Article
- Immunomodulation Using BMP-7 and IL-10 to Enhance the Mineralization Capacity of Bone Progenitor Cells in a Fracture Hematoma-Like Environment.Advanced healthcare materials · 2025Article
- Effects of Hypomethylating Agents on Gene Modulation in the Leukemic Microenvironment and Disease Trajectory in a Mouse Model of AML.bioRxiv : the preprint server for biology · 2024Article
- Cell autonomous functions of CD47 in regulating cellular plasticity and metabolic plasticity.Cell death and differentiation · 2024Review
- Data-independent LC-MS/MS analysis of ME/CFS plasma reveals a dysregulated coagulation system, endothelial dysfunction, downregulation of complement machinery.Cardiovascular diabetology · 2024Article
- Nociceptor-immune interactomes reveal insult-specific immune signatures of pain.Nature immunology · 2024Article
- Progress in cancer research on the regulator of phagocytosis CD47, which determines the fate of tumor cells (Review).Oncology letters · 2024Review
- Macromolecular crowding in human tenocyte and skin fibroblast cultures: A comparative analysis.Materials today. Bio · 2024Article
57 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Platelet alpha-granules constitute the major rapidly releasable reservoir of thrombospondin-1 in higher animals. Although some fragments and peptides derived from thrombospondin-1 stimulate or inhibit platelet aggregation, its physiologic function in platelets has remained elusive. We now show that endogenous thrombospondin-1 is necessary for platelet aggregation in vitro in the presence of physiologic levels of nitric oxide (NO). Exogenous NO or elevation of cGMP delays thrombin-induced platelet aggregation under high shear and static conditions, and exogenous thrombospondin-1 reverses this delay. Thrombospondin-1-null murine platelets fail to aggregate in response to thrombin in the presence of exogenous NO or 8Br-cGMP. At physiologic concentrations of the NO synthase substrate arginine, thrombospondin-1-null platelets have elevated basal cGMP. Ligation of CD36 or CD47 is sufficient to block NO-induced cGMP accumulation and mimic the effect of thrombospondin-1 on aggregation. Exogenous thrombospondin-1 also reverses the suppression by NO of alphaIIb/beta3 integrin-mediated platelet adhesion on immobilized fibrinogen, mediated in part by increased GTP loading of Rap1. Thrombospondin-1 also inhibits cGMP-mediated activation of cGMP-dependent protein kinase and thereby prevents phosphorylation of VASP. Thus, release of thrombospondin-1 from alpha-granules during activation provides positive feedback to promote efficient platelet aggregation and adhesion by overcoming the antithrombotic activity of physiologic NO.
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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.