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Effects of extracellular DNA on plasminogen activation and fibrinolysis

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TLDR
Extracellular DNA at physiological concentrations may potentiate fibrinolysis by stimulating fibrin-independent plasminogen activation and increases enzyme susceptibility to serpins, and DNA is a macromolecular template that both potentiates and inhibits fibrinelysis.
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This article is published in Journal of Biological Chemistry.The article was published on 2011-12-09 and is currently open access. It has received 54 citations till now. The article focuses on the topics: Plasminogen activator & Plasmin.

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Mechanical Stability and Fibrinolytic Resistance of Clots Containing Fibrin, DNA, and Histones

TL;DR: It is demonstrated that the addition of histone-DNA complexes to fibrin results in thicker fibers accompanied by improved stability and rigidity, and Therapeutic strategies could be optimized to enhance fibrinolysis in clots containing DNA and histones.
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The role of leukocytes in thrombosis.

TL;DR: Modulation of the interactions between leukocytes or leukocyte-derived procoagulant materials and the traditional hemostatic system is an attractive target for the development of novel antithrombotic strategies.
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Extracellular DNA and histones: double-edged swords in immunothrombosis.

TL;DR: The pathologic nature ofcfDNA and histones in macrovascular and microvascular thrombosis, including venous thromboembolism, cancer, sepsis, and trauma is reviewed and the prognostic value of cfDNA andhistones in these disease states is discussed.
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DAMP and DIC: The role of extracellular DNA and DNA-binding proteins in the pathogenesis of DIC

TL;DR: The present review gives an overview on how extracellular DNA is released into circulation and the structure of circulating DNA and summarizes the effect of ext racellular DNA and DNA-binding proteins on platelet activation, plasmatic coagulation as well as fibrinolysis.
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Cell-Free DNA Modulates Clot Structure and Impairs Fibrinolysis in Sepsis

TL;DR: The studies suggest that the increased levels of CFDNA in sepsis impair fibrinolysis by inhibiting plasmin-mediated fibrin degradation, thereby identifying CFDNA as a potential therapeutic target for sepsi treatment.
References
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Journal ArticleDOI

Extracellular DNA traps promote thrombosis

TL;DR: It is reported that NETs provide a heretofore unrecognized scaffold and stimulus for thrombus formation and may further explain the epidemiological association of infection with thrombosis.
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Serine protease mechanism and specificity

TL;DR: This article will review recent work on the mechanism and specificity of chymotrypsin-like enzymes, with the occasional references to pertinent experiments with subtilisin.
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Kinetics of the activation of plasminogen by human tissue plasminogen activator. Role of fibrin.

TL;DR: The kinetic analysis suggested that the activation in the presence of fibrin occurs through binding of an activator molecule to the clot surface and subsequent addition of plasminogen (sequential ordered mechanism) to form a cyclic ternary complex.

Kinetics of the Activation of Plasminogen by Human Tissue Plasminogen Activator

TL;DR: In this paper, the activation of Gluplasminogen and Lys-minminogen in the presence of fibrinogen (f) was studied in purified systems, and the initial rate of activation (u) was calculated.
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U.K. Controlled trial of intrapleural streptokinase for pleural infection.

TL;DR: The intrapleural administration of streptokinase does not improve mortality, the rate of surgery, or the length of the hospital stay among patients with pleural infection.
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