ArticleFrontiers in immunology2017
The Procoagulant Activity of Apoptotic Cells Is Mediated by Interaction with Factor XII.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Design of Apoptotic Cell-Inspired Particles as a Blood Coagulation Test.Biomimetics (Basel, Switzerland) · 2024Article
- Pathophysiology of Coagulation and Emerging Roles for Extracellular Vesicles in Coagulation Cascades and Disorders.Journal of clinical medicine · 2022Review
- Association of FXI activity with thrombo-inflammation, extracellular matrix, lipid metabolism and apoptosis in venous thrombosis.Scientific reports · 2022Article
- Novel interaction of properdin and coagulation factor XI: Crosstalk between complement and coagulation.Research and practice in thrombosis and haemostasis · 2022Article
- Extracellular Vesicles and Thrombosis: Update on the Clinical and Experimental Evidence.International journal of molecular sciences · 2021Review
- The contact system in liver injury.Seminars in immunopathology · 2021Review
- The SARS-CoV-2/Receptor Axis in Heart and Blood Vessels: A Crisp Update on COVID-19 Disease with Cardiovascular Complications.Viruses · 2021Review
- Beta-2-Glycoprotein-I Deficiency Could Precipitate an Antiphospholipid Syndrome-like Prothrombotic Situation in Patients With Coronavirus Disease 2019.ACR open rheumatology · 2021Article
- Complement Deficiencies Result in Surrogate Pathways of Complement Activation in Novel Polygenic Lupus-like Models of Kidney Injury.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Article
- Influence of factor XII deficiency on activated partial thromboplastin time (aPTT) in critically ill patients.Journal of thrombosis and thrombolysis · 2019Article
- Zika Virus Infection Induces Elevation of Tissue Factor Production and Apoptosis on Human Umbilical Vein Endothelial Cells.Frontiers in microbiology · 2019Article
- The Plasma Kallikrein-Kininogen Pathway Is Critical in the Pathogenesis of Colitis in Mice.Frontiers in immunology · 2018Article
- Endothelial Dysfunction in Kidney Transplantation.Frontiers in immunology · 2018Review
- Hemodialysis-Related Complement and Contact Pathway Activation and Cardiovascular Risk: A Narrative Review.Kidney medicineReview
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptotic cells, by externalizing phosphatidylserine (PS) as a hallmark feature, are procoagulant. However, the mechanism by which apoptotic cells activate coagulation system remains unknown. Intrinsic coagulation pathway is initiated by coagulation factor XII (FXII) of contact activation system. The purpose of this study was to determine whether FXII is involved in procoagulant activity of apoptotic cells. Using western blotting and chromogenic substrate assay, we found that incubation with apoptotic cells, but not with viable cells, resulted in rapid cleavage and activation of FXII in the presence of prekallikrein and high molecular weight kininogen (HK), other two components of contact activation system. As detected by flow cytometry, FXII bound to apoptotic cells in a concentration-dependent manner, which was inhibited by annexin V and PS liposome. Direct association of FXII with PS was confirmed in a surface plasmon resonance assay. Clotting time of FXII-deficient plasma induced by apoptotic cells was significantly prolonged, which was fully reversed by replenishment with FXII. Corn trypsin inhibitor, a FXII inhibitor, completely prevented apoptotic cells-induced intrinsic tenase complex formation. Consistently, apoptotic cells significantly increased thrombin production in normal plasma, which was not affected by an inhibitory anti-tissue factor antibody. However, blocking of PS by annexin V, inhibition of FXII, or the deficiency of FXII suppressed apoptotic cells-induced thrombin generation. Addition of purified FXII to FXII-deficient plasma recovered thrombin generation to the normal plasma level. In conclusion, FXII binds to apoptotic cells
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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.