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Platelets promote coagulation factor XII-mediated proteolytic cascade systems in plasma

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Platelets promote coagulation factor XII-mediated proteolytic cascade systems in plasma. / Johne, Julia; Blume, Constanze; Benz, Peter M; Pozgajová, Miroslava; Ullrich, Melanie; Schuh, Kai; Nieswandt, Bernhard; Walter, Ulrich; Renné, Thomas.

In: BIOL CHEM, Vol. 387, No. 2, 01.02.2006, p. 173-8.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Johne, J, Blume, C, Benz, PM, Pozgajová, M, Ullrich, M, Schuh, K, Nieswandt, B, Walter, U & Renné, T 2006, 'Platelets promote coagulation factor XII-mediated proteolytic cascade systems in plasma', BIOL CHEM, vol. 387, no. 2, pp. 173-8. https://doi.org/10.1515/BC.2006.023

APA

Johne, J., Blume, C., Benz, P. M., Pozgajová, M., Ullrich, M., Schuh, K., Nieswandt, B., Walter, U., & Renné, T. (2006). Platelets promote coagulation factor XII-mediated proteolytic cascade systems in plasma. BIOL CHEM, 387(2), 173-8. https://doi.org/10.1515/BC.2006.023

Vancouver

Johne J, Blume C, Benz PM, Pozgajová M, Ullrich M, Schuh K et al. Platelets promote coagulation factor XII-mediated proteolytic cascade systems in plasma. BIOL CHEM. 2006 Feb 1;387(2):173-8. https://doi.org/10.1515/BC.2006.023

Bibtex

@article{56b1ddf4fa66435693146e7830ea1c7f,
title = "Platelets promote coagulation factor XII-mediated proteolytic cascade systems in plasma",
abstract = "Blood coagulation factor XII (FXII, Hageman factor) is a plasma serine protease which is autoactivated following contact with negatively charged surfaces in a reaction involving plasma kallikrein and high-molecular-weight kininogen (contact phase activation). Active FXII has the ability to initiate blood clotting via the intrinsic pathway of coagulation and inflammatory reactions via the kallikrein-kinin system. Here we have determined FXII-mediated bradykinin formation and clotting in plasma. Western blotting analysis with specific antibodies against various parts of the contact factors revealed that limited activation of FXII is sufficient to promote plasma kallikrein activation, resulting in the conversion of high-molecular-weight kininogen and bradykinin generation. The presence of platelets significantly promoted FXII-initiated bradykinin formation. Similarly, in vitro clotting assays revealed that platelets critically promoted FXII-driven thrombin and fibrin formation. In summary, our data suggest that FXII-initiated protease cascades may proceed on platelet surfaces, with implications for inflammation and clotting.",
keywords = "Blood Coagulation, Blood Platelets, Bradykinin, Factor XII, Humans, Kallikrein-Kinin System, Kininogens, Molecular Weight, Reference Values, Thrombin, Time Factors",
author = "Julia Johne and Constanze Blume and Benz, {Peter M} and Miroslava Pozgajov{\'a} and Melanie Ullrich and Kai Schuh and Bernhard Nieswandt and Ulrich Walter and Thomas Renn{\'e}",
year = "2006",
month = feb,
day = "1",
doi = "10.1515/BC.2006.023",
language = "English",
volume = "387",
pages = "173--8",
journal = "BIOL CHEM",
issn = "1431-6730",
publisher = "Walter de Gruyter GmbH & Co. KG",
number = "2",

}

RIS

TY - JOUR

T1 - Platelets promote coagulation factor XII-mediated proteolytic cascade systems in plasma

AU - Johne, Julia

AU - Blume, Constanze

AU - Benz, Peter M

AU - Pozgajová, Miroslava

AU - Ullrich, Melanie

AU - Schuh, Kai

AU - Nieswandt, Bernhard

AU - Walter, Ulrich

AU - Renné, Thomas

PY - 2006/2/1

Y1 - 2006/2/1

N2 - Blood coagulation factor XII (FXII, Hageman factor) is a plasma serine protease which is autoactivated following contact with negatively charged surfaces in a reaction involving plasma kallikrein and high-molecular-weight kininogen (contact phase activation). Active FXII has the ability to initiate blood clotting via the intrinsic pathway of coagulation and inflammatory reactions via the kallikrein-kinin system. Here we have determined FXII-mediated bradykinin formation and clotting in plasma. Western blotting analysis with specific antibodies against various parts of the contact factors revealed that limited activation of FXII is sufficient to promote plasma kallikrein activation, resulting in the conversion of high-molecular-weight kininogen and bradykinin generation. The presence of platelets significantly promoted FXII-initiated bradykinin formation. Similarly, in vitro clotting assays revealed that platelets critically promoted FXII-driven thrombin and fibrin formation. In summary, our data suggest that FXII-initiated protease cascades may proceed on platelet surfaces, with implications for inflammation and clotting.

AB - Blood coagulation factor XII (FXII, Hageman factor) is a plasma serine protease which is autoactivated following contact with negatively charged surfaces in a reaction involving plasma kallikrein and high-molecular-weight kininogen (contact phase activation). Active FXII has the ability to initiate blood clotting via the intrinsic pathway of coagulation and inflammatory reactions via the kallikrein-kinin system. Here we have determined FXII-mediated bradykinin formation and clotting in plasma. Western blotting analysis with specific antibodies against various parts of the contact factors revealed that limited activation of FXII is sufficient to promote plasma kallikrein activation, resulting in the conversion of high-molecular-weight kininogen and bradykinin generation. The presence of platelets significantly promoted FXII-initiated bradykinin formation. Similarly, in vitro clotting assays revealed that platelets critically promoted FXII-driven thrombin and fibrin formation. In summary, our data suggest that FXII-initiated protease cascades may proceed on platelet surfaces, with implications for inflammation and clotting.

KW - Blood Coagulation

KW - Blood Platelets

KW - Bradykinin

KW - Factor XII

KW - Humans

KW - Kallikrein-Kinin System

KW - Kininogens

KW - Molecular Weight

KW - Reference Values

KW - Thrombin

KW - Time Factors

U2 - 10.1515/BC.2006.023

DO - 10.1515/BC.2006.023

M3 - SCORING: Journal article

C2 - 16497149

VL - 387

SP - 173

EP - 178

JO - BIOL CHEM

JF - BIOL CHEM

SN - 1431-6730

IS - 2

ER -