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Defective thrombus formation in mice lacking coagulation factor XII

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Defective thrombus formation in mice lacking coagulation factor XII. / Renné, Thomas; Pozgajová, Miroslava; Grüner, Sabine; Schuh, Kai; Pauer, Hans-Ulrich; Burfeind, Peter; Gailani, David; Nieswandt, Bernhard.

in: J EXP MED, Jahrgang 202, Nr. 2, 18.07.2005, S. 271-81.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Renné, T, Pozgajová, M, Grüner, S, Schuh, K, Pauer, H-U, Burfeind, P, Gailani, D & Nieswandt, B 2005, 'Defective thrombus formation in mice lacking coagulation factor XII', J EXP MED, Jg. 202, Nr. 2, S. 271-81. https://doi.org/10.1084/jem.20050664

APA

Renné, T., Pozgajová, M., Grüner, S., Schuh, K., Pauer, H-U., Burfeind, P., Gailani, D., & Nieswandt, B. (2005). Defective thrombus formation in mice lacking coagulation factor XII. J EXP MED, 202(2), 271-81. https://doi.org/10.1084/jem.20050664

Vancouver

Renné T, Pozgajová M, Grüner S, Schuh K, Pauer H-U, Burfeind P et al. Defective thrombus formation in mice lacking coagulation factor XII. J EXP MED. 2005 Jul 18;202(2):271-81. https://doi.org/10.1084/jem.20050664

Bibtex

@article{f61cca94a2fb4e40b40b2ee027163bb7,
title = "Defective thrombus formation in mice lacking coagulation factor XII",
abstract = "Blood coagulation is thought to be initiated by plasma protease factor VIIa in complex with the membrane protein tissue factor. In contrast, coagulation factor XII (FXII)-mediated fibrin formation is not believed to play an important role for coagulation in vivo. We used FXII-deficient mice to study the contributions of FXII to thrombus formation in vivo. Intravital fluorescence microscopy and blood flow measurements in three distinct arterial beds revealed a severe defect in the formation and stabilization of platelet-rich occlusive thrombi. Although FXII-deficient mice do not experience spontaneous or excessive injury-related bleeding, they are protected against collagen- and epinephrine-induced thromboembolism. Infusion of human FXII into FXII-null mice restored injury-induced thrombus formation. These unexpected findings change the long-standing concept that the FXII-induced intrinsic coagulation pathway is not important for clotting in vivo. The results establish FXII as essential for thrombus formation, and identify FXII as a novel target for antithrombotic therapy.",
keywords = "Animals, Blood Coagulation, Collagen, Epinephrine, Factor VIIa, Factor XII Deficiency, Factor XIIa, Hemorrhage, Lung, Mice, Mice, Mutant Strains, Platelet Aggregation, Thromboembolism, Vasoconstrictor Agents",
author = "Thomas Renn{\'e} and Miroslava Pozgajov{\'a} and Sabine Gr{\"u}ner and Kai Schuh and Hans-Ulrich Pauer and Peter Burfeind and David Gailani and Bernhard Nieswandt",
year = "2005",
month = jul,
day = "18",
doi = "10.1084/jem.20050664",
language = "English",
volume = "202",
pages = "271--81",
journal = "J EXP MED",
issn = "0022-1007",
publisher = "Rockefeller University Press",
number = "2",

}

RIS

TY - JOUR

T1 - Defective thrombus formation in mice lacking coagulation factor XII

AU - Renné, Thomas

AU - Pozgajová, Miroslava

AU - Grüner, Sabine

AU - Schuh, Kai

AU - Pauer, Hans-Ulrich

AU - Burfeind, Peter

AU - Gailani, David

AU - Nieswandt, Bernhard

PY - 2005/7/18

Y1 - 2005/7/18

N2 - Blood coagulation is thought to be initiated by plasma protease factor VIIa in complex with the membrane protein tissue factor. In contrast, coagulation factor XII (FXII)-mediated fibrin formation is not believed to play an important role for coagulation in vivo. We used FXII-deficient mice to study the contributions of FXII to thrombus formation in vivo. Intravital fluorescence microscopy and blood flow measurements in three distinct arterial beds revealed a severe defect in the formation and stabilization of platelet-rich occlusive thrombi. Although FXII-deficient mice do not experience spontaneous or excessive injury-related bleeding, they are protected against collagen- and epinephrine-induced thromboembolism. Infusion of human FXII into FXII-null mice restored injury-induced thrombus formation. These unexpected findings change the long-standing concept that the FXII-induced intrinsic coagulation pathway is not important for clotting in vivo. The results establish FXII as essential for thrombus formation, and identify FXII as a novel target for antithrombotic therapy.

AB - Blood coagulation is thought to be initiated by plasma protease factor VIIa in complex with the membrane protein tissue factor. In contrast, coagulation factor XII (FXII)-mediated fibrin formation is not believed to play an important role for coagulation in vivo. We used FXII-deficient mice to study the contributions of FXII to thrombus formation in vivo. Intravital fluorescence microscopy and blood flow measurements in three distinct arterial beds revealed a severe defect in the formation and stabilization of platelet-rich occlusive thrombi. Although FXII-deficient mice do not experience spontaneous or excessive injury-related bleeding, they are protected against collagen- and epinephrine-induced thromboembolism. Infusion of human FXII into FXII-null mice restored injury-induced thrombus formation. These unexpected findings change the long-standing concept that the FXII-induced intrinsic coagulation pathway is not important for clotting in vivo. The results establish FXII as essential for thrombus formation, and identify FXII as a novel target for antithrombotic therapy.

KW - Animals

KW - Blood Coagulation

KW - Collagen

KW - Epinephrine

KW - Factor VIIa

KW - Factor XII Deficiency

KW - Factor XIIa

KW - Hemorrhage

KW - Lung

KW - Mice

KW - Mice, Mutant Strains

KW - Platelet Aggregation

KW - Thromboembolism

KW - Vasoconstrictor Agents

U2 - 10.1084/jem.20050664

DO - 10.1084/jem.20050664

M3 - SCORING: Journal article

C2 - 16009717

VL - 202

SP - 271

EP - 281

JO - J EXP MED

JF - J EXP MED

SN - 0022-1007

IS - 2

ER -