ArticleBlood2015
Plasminogen associates with phosphatidylserine-exposing platelets and contributes to thrombus lysis under flow.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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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.
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Who cites it
45 citing papers in PubMed, 121 citations in OpenAlex.
- A multi-omics approach investigating thrombolysis resistance in acute ischemic stroke thrombi.Journal of thrombosis and thrombolysis · 2026Article
- Plg-RMolecular medicine (Cambridge, Mass.) · 2026Article
- Automated Imaging and Analysis of Platelet, Coagulation and Fibrinolysis Activities Using a Novel Flow Chip-Based System at Physiological Temperature.Micromachines · 2025Article
- Dissolving porcine and human microthrombi by short exposure to microdoses of alteplase in an in vitro model of microvascular obstruction.Scientific reports · 2025Article
- Injury-on-a-chip for modelling microvascular trauma-induced coagulation.Lab on a chip · 2025Article
- Phosphatidylserine: A Novel Target for Ischemic Stroke Treatment.Biomolecules · 2024Review
- Activated platelets retain and protect most of their factor XIII-A cargo from proteolytic activation and degradation.Blood advances · 2024Article
- Article
- Platelet factor XIII-A regulates platelet function and promotes clot retraction and stability.Research and practice in thrombosis and haemostasis · 2023Article
- Real-time tracking of fibrinolysis under constant wall shear and various pulsatile flows in an in-vitro thrombolysis model.Bioengineering & translational medicine · 2023Article
- Thrombus composition and thrombolysis resistance in stroke.Research and practice in thrombosis and haemostasis · 2023Article
- Point-of-care diagnosis and monitoring of fibrinolysis resistance in the critically ill: results from a feasibility study.Critical care (London, England) · 2023Article
- All tangled up: interactions of the fibrinolytic and innate immune systems.Frontiers in medicine · 2023Review
- Determinants of Endogenous Fibrinolysis in Whole Blood Under High Shear in Patients With Myocardial Infarction.JACC. Basic to translational science · 2022Article
- Review
- Role of Plasminogen Activation System in Platelet Pathophysiology: Emerging Concepts for Translational Applications.International journal of molecular sciences · 2022Review
- Hirudin promotes proliferation and osteogenic differentiation of HBMSCs via activation of cyclic guanosine monophosphate (cGMP)/protein kinase-G (PKG) signaling pathway.Bioengineered · 2022Article
- Location, location, location: Fibrin, cells, and fibrinolytic factors in thrombi.Frontiers in cardiovascular medicine · 2022Review
- "Going with the flow" in modeling fibrinolysis.Frontiers in cardiovascular medicine · 2022Review
- Composition and Organization of Acute Ischemic Stroke Thrombus: A Wealth of Information for Future Thrombolytic Strategies.Frontiers in neurology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The interaction of plasminogen with platelets and their localization during thrombus formation and fibrinolysis under flow are not defined. Using a novel model of whole blood thrombi, formed under flow, we examine dose-dependent fibrinolysis using fluorescence microscopy. Fibrinolysis was dependent upon flow and the balance between fibrin formation and plasminogen activation, with tissue plasminogen activator-mediated lysis being more efficient than urokinase plasminogen activator-mediated lysis. Fluorescently labeled plasminogen radiates from platelet aggregates at the base of thrombi, primarily in association with fibrin. Hirudin attenuates, but does not abolish plasminogen binding, denoting the importance of fibrin. Flow cytometry revealed that stimulation of platelets with thrombin/convulxin significantly increased the plasminogen signal associated with phosphatidylserine (PS)-exposing platelets. Binding was attenuated by tirofiban and Gly-Pro-Arg-Pro amide, confirming a role for fibrin in amplifying plasminogen binding to PS-exposing platelets. Confocal microscopy revealed direct binding of plasminogen and fibrinogen to different platelet subpopulations. Binding of plasminogen and fibrinogen co-localized with PAC-1 in the center of spread platelets. In contrast, PS-exposing platelets were PAC-1 negative, and bound plasminogen and fibrinogen in a protruding "cap." These data show that different subpopulations of platelets harbor plasminogen by diverse mechanisms and provide an essential scaffold for the accumulation of fibrinolytic proteins that mediate fibrinolysis under flow.
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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.