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http://dx.doi.org/10.1016/j.ajog.2016.02.014 | DOI Listing |
J Vis Exp
November 2024
Department of Haematology, University Hospital of Bordeaux; Inserm U1034, Biology of Cardiovascular Disease.
Activated platelets promote coagulation primarily by exposing the procoagulant phospholipid phosphatidylserine (PS) on their outer membrane surfaces and releasing PS-expressing microvesicles that retain the original membrane architecture and cytoplasmic components of their originating cells. The accessibility of phosphatidylserine facilitates the binding of major coagulation factors, significantly amplifying the catalytic efficiency of coagulation enzymes, while microvesicle release acts as a pivotal mediator of intercellular signaling. Procoagulant platelets play a crucial role in clot stabilization during hemostasis, and their increased proportion in the bloodstream correlates with an increased risk of thrombosis.
View Article and Find Full Text PDFThromb Res
December 2024
Department of Bioengineering, College of Engineering and Computing, George Mason University, Manassas, VA 20110, United States of America. Electronic address:
Introduction: Acute respiratory distress syndrome (ARDS) patients are at risk of thrombosis through mechanisms implicating oxidized low-density lipoprotein (oxLDL). Endothelial cells, immune cells and platelets were reported to express scavenger receptors for oxLDL: Lox-1 and CD36. We hypothesized that platelets shed a soluble Lox-1 ectodomain (sLox-1) and release CD36-bearing procoagulant microparticles (MPs), that both become elevated in subjects with ARDS-induced coagulopathy.
View Article and Find Full Text PDFCell Signal
December 2024
Centre for Blood Research, University of British Columbia, Vancouver, BC, Canada; Department of Oral Biological and Medical Sciences, University of British Columbia, Vancouver, BC, Canada; Department of Biochemistry and Molecular Biology, University of British Columbia, Vancouver, BC, Canada. Electronic address:
Upon activation by vascular injury or extracellular agonists, platelets undergo rapid change shape, a process regulated by the actin cytoskeleton and accessory proteins. Platelet shape change is accompanied by the secretion of hemostatic factors and immunomodulatory cytokines from their intracellular granules, as well as the release of microvesicles (MVs) containing pro-inflammatory cytokines and procoagulant phosphatidylserine (PS). However, the role of actin dynamics in MV generation remains unclear.
View Article and Find Full Text PDFJ Thromb Haemost
December 2024
Centre for Blood Research, Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada; Division of Medical Affairs and Innovation, Canadian Blood Services, Ottawa, Ontario, Canada.
Many virus types affect the blood clotting system with correlations to pathology that range widely from thrombosis to hemorrhage linking to inflammation. Here we overview the intricate crosstalk induced by infection between proteins on the virus encoded by either the host or virus genomes, coagulation proteins, platelets, leukocytes, and endothelial cells. For blood-borne viruses with an outer covering acquired from the host cell, the envelope, a key player may be the cell-derived trigger of coagulation on the virus surface, tissue factor (TF).
View Article and Find Full Text PDFZhonghua Wei Zhong Bing Ji Jiu Yi Xue
July 2024
Department of Critical Care Medicine, the First Affiliated Hospital of Harbin Medical University, Harbin 150001, Heilongjiang, China. Corresponding author: Meng Shishuai, Email:
Objective: To investigate the characteristic of circulating microparticle in patients with acute myocardial infarction (AMI) and its possible mechanism of promoting coagulation.
Methods: A prospective case-control study was conducted. The patients with coronary heart disease admitted to the second department of cardiology in Harbin First Hospital from June to November 2023 were enrolled, and they were grouped according to whether the patients occurred AMI or not.
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