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, Jahrgang 387, Nr. 2, 01.02.2006, S. 173-8.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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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 -