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A role for factor XIIa-mediated factor XI activation in thrombus formation in vivo.

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A role for factor XIIa-mediated factor XI activation in thrombus formation in vivo. / Cheng, Qiufang; Tucker, Erik I; Pine, Meghann S; Sisler, India; Matafonov, Anton; Sun, Mao-Fu; White-Adams, Tara C; Smith, Stephanie A; Hanson, Stephen R; McCarty, Owen J T; Renné, Thomas; Gruber, András; Gailani, David.

in: BLOOD, Jahrgang 116, Nr. 19, 19, 2010, S. 3981-3989.

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

Harvard

Cheng, Q, Tucker, EI, Pine, MS, Sisler, I, Matafonov, A, Sun, M-F, White-Adams, TC, Smith, SA, Hanson, SR, McCarty, OJT, Renné, T, Gruber, A & Gailani, D 2010, 'A role for factor XIIa-mediated factor XI activation in thrombus formation in vivo.', BLOOD, Jg. 116, Nr. 19, 19, S. 3981-3989. <http://www.ncbi.nlm.nih.gov/pubmed/20634381?dopt=Citation>

APA

Cheng, Q., Tucker, E. I., Pine, M. S., Sisler, I., Matafonov, A., Sun, M-F., White-Adams, T. C., Smith, S. A., Hanson, S. R., McCarty, O. J. T., Renné, T., Gruber, A., & Gailani, D. (2010). A role for factor XIIa-mediated factor XI activation in thrombus formation in vivo. BLOOD, 116(19), 3981-3989. [19]. http://www.ncbi.nlm.nih.gov/pubmed/20634381?dopt=Citation

Vancouver

Cheng Q, Tucker EI, Pine MS, Sisler I, Matafonov A, Sun M-F et al. A role for factor XIIa-mediated factor XI activation in thrombus formation in vivo. BLOOD. 2010;116(19):3981-3989. 19.

Bibtex

@article{a680c573ab044ad7ba983bd52c17cb2c,
title = "A role for factor XIIa-mediated factor XI activation in thrombus formation in vivo.",
abstract = "Mice lacking factor XII (fXII) or factor XI (fXI) are resistant to experimentally-induced thrombosis, suggesting fXIIa activation of fXI contributes to thrombus formation in vivo. It is not clear whether this reaction has relevance for thrombosis in pri mates. In 2 carotid artery injury models (FeCl(3) and Rose Bengal/laser), fXII-deficient mice are more resistant to thrombosis than fXI- or factor IX (fIX)-deficient mice, raising the possibility that fXII and fXI function in distinct pathways. Antibody 14E11 binds fXI from a variety of mammals and interferes with fXI activation by fXIIa in vitro. In mice, 14E11 prevented arterial occlusion induced by FeCl(3) to a similar degree to total fXI deficiency. 14E11 also had a modest beneficial effect in a tissue factor-induced pulmonary embolism model, indicating fXI and fXII contribute to thrombus formation even when factor VIIa/tissue factor initiates thrombosis. In baboons, 14E11 reduced platelet-rich thrombus growth in collagen-coated grafts inserted into an arteriovenous shunt. These data support the hypothesis that fXIIa-mediated fXI activation contributes to thrombus formation in rodents and primates. Since fXII deficiency does not impair hemostasis, targeted inhibition of fXI activation by fXIIa may be a useful antithrombotic strategy associated with a low risk of bleeding complications.",
keywords = "Animals, Humans, Male, Disease Models, Animal, Mice, Mice, Inbred BALB C, Mice, Knockout, Dogs, Rabbits, Species Specificity, Antibodies, Monoclonal/pharmacology, Cats, Factor XIIa/*physiology, Anticoagulants/pharmacology, Carotid Artery Thrombosis/blood/etiology, Factor XI/antagonists & inhibitors/*physiology, Factor XI Deficiency/blood/genetics/physiopathology, Factor XII Deficiency/blood/genetics/physiopathology, Papio anubis, Partial Thromboplastin Time, Pulmonary Embolism/blood/etiology, Thrombosis/*blood/*etiology, Animals, Humans, Male, Disease Models, Animal, Mice, Mice, Inbred BALB C, Mice, Knockout, Dogs, Rabbits, Species Specificity, Antibodies, Monoclonal/pharmacology, Cats, Factor XIIa/*physiology, Anticoagulants/pharmacology, Carotid Artery Thrombosis/blood/etiology, Factor XI/antagonists & inhibitors/*physiology, Factor XI Deficiency/blood/genetics/physiopathology, Factor XII Deficiency/blood/genetics/physiopathology, Papio anubis, Partial Thromboplastin Time, Pulmonary Embolism/blood/etiology, Thrombosis/*blood/*etiology",
author = "Qiufang Cheng and Tucker, {Erik I} and Pine, {Meghann S} and India Sisler and Anton Matafonov and Mao-Fu Sun and White-Adams, {Tara C} and Smith, {Stephanie A} and Hanson, {Stephen R} and McCarty, {Owen J T} and Thomas Renn{\'e} and Andr{\'a}s Gruber and David Gailani",
year = "2010",
language = "English",
volume = "116",
pages = "3981--3989",
journal = "BLOOD",
issn = "0006-4971",
publisher = "American Society of Hematology",
number = "19",

}

RIS

TY - JOUR

T1 - A role for factor XIIa-mediated factor XI activation in thrombus formation in vivo.

AU - Cheng, Qiufang

AU - Tucker, Erik I

AU - Pine, Meghann S

AU - Sisler, India

AU - Matafonov, Anton

AU - Sun, Mao-Fu

AU - White-Adams, Tara C

AU - Smith, Stephanie A

AU - Hanson, Stephen R

AU - McCarty, Owen J T

AU - Renné, Thomas

AU - Gruber, András

AU - Gailani, David

PY - 2010

Y1 - 2010

N2 - Mice lacking factor XII (fXII) or factor XI (fXI) are resistant to experimentally-induced thrombosis, suggesting fXIIa activation of fXI contributes to thrombus formation in vivo. It is not clear whether this reaction has relevance for thrombosis in pri mates. In 2 carotid artery injury models (FeCl(3) and Rose Bengal/laser), fXII-deficient mice are more resistant to thrombosis than fXI- or factor IX (fIX)-deficient mice, raising the possibility that fXII and fXI function in distinct pathways. Antibody 14E11 binds fXI from a variety of mammals and interferes with fXI activation by fXIIa in vitro. In mice, 14E11 prevented arterial occlusion induced by FeCl(3) to a similar degree to total fXI deficiency. 14E11 also had a modest beneficial effect in a tissue factor-induced pulmonary embolism model, indicating fXI and fXII contribute to thrombus formation even when factor VIIa/tissue factor initiates thrombosis. In baboons, 14E11 reduced platelet-rich thrombus growth in collagen-coated grafts inserted into an arteriovenous shunt. These data support the hypothesis that fXIIa-mediated fXI activation contributes to thrombus formation in rodents and primates. Since fXII deficiency does not impair hemostasis, targeted inhibition of fXI activation by fXIIa may be a useful antithrombotic strategy associated with a low risk of bleeding complications.

AB - Mice lacking factor XII (fXII) or factor XI (fXI) are resistant to experimentally-induced thrombosis, suggesting fXIIa activation of fXI contributes to thrombus formation in vivo. It is not clear whether this reaction has relevance for thrombosis in pri mates. In 2 carotid artery injury models (FeCl(3) and Rose Bengal/laser), fXII-deficient mice are more resistant to thrombosis than fXI- or factor IX (fIX)-deficient mice, raising the possibility that fXII and fXI function in distinct pathways. Antibody 14E11 binds fXI from a variety of mammals and interferes with fXI activation by fXIIa in vitro. In mice, 14E11 prevented arterial occlusion induced by FeCl(3) to a similar degree to total fXI deficiency. 14E11 also had a modest beneficial effect in a tissue factor-induced pulmonary embolism model, indicating fXI and fXII contribute to thrombus formation even when factor VIIa/tissue factor initiates thrombosis. In baboons, 14E11 reduced platelet-rich thrombus growth in collagen-coated grafts inserted into an arteriovenous shunt. These data support the hypothesis that fXIIa-mediated fXI activation contributes to thrombus formation in rodents and primates. Since fXII deficiency does not impair hemostasis, targeted inhibition of fXI activation by fXIIa may be a useful antithrombotic strategy associated with a low risk of bleeding complications.

KW - Animals

KW - Humans

KW - Male

KW - Disease Models, Animal

KW - Mice

KW - Mice, Inbred BALB C

KW - Mice, Knockout

KW - Dogs

KW - Rabbits

KW - Species Specificity

KW - Antibodies, Monoclonal/pharmacology

KW - Cats

KW - Factor XIIa/physiology

KW - Anticoagulants/pharmacology

KW - Carotid Artery Thrombosis/blood/etiology

KW - Factor XI/antagonists & inhibitors/physiology

KW - Factor XI Deficiency/blood/genetics/physiopathology

KW - Factor XII Deficiency/blood/genetics/physiopathology

KW - Papio anubis

KW - Partial Thromboplastin Time

KW - Pulmonary Embolism/blood/etiology

KW - Thrombosis/blood/etiology

KW - Animals

KW - Humans

KW - Male

KW - Disease Models, Animal

KW - Mice

KW - Mice, Inbred BALB C

KW - Mice, Knockout

KW - Dogs

KW - Rabbits

KW - Species Specificity

KW - Antibodies, Monoclonal/pharmacology

KW - Cats

KW - Factor XIIa/physiology

KW - Anticoagulants/pharmacology

KW - Carotid Artery Thrombosis/blood/etiology

KW - Factor XI/antagonists & inhibitors/physiology

KW - Factor XI Deficiency/blood/genetics/physiopathology

KW - Factor XII Deficiency/blood/genetics/physiopathology

KW - Papio anubis

KW - Partial Thromboplastin Time

KW - Pulmonary Embolism/blood/etiology

KW - Thrombosis/blood/etiology

M3 - SCORING: Journal article

VL - 116

SP - 3981

EP - 3989

JO - BLOOD

JF - BLOOD

SN - 0006-4971

IS - 19

M1 - 19

ER -