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Targeted deletion of murine coagulation factor XII gene-a model for contact phase activation in vivo

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Targeted deletion of murine coagulation factor XII gene-a model for contact phase activation in vivo. / Pauer, Hans-Ulrich; Renné, Thomas; Hemmerlein, Bernhard; Legler, Tobias; Fritzlar, Saskia; Adham, Ibrahim; Müller-Esterl, Werner; Emons, Guenter; Sancken, Ulrich; Engel, Wolfgang; Burfeind, Peter.

In: THROMB HAEMOSTASIS, Vol. 92, No. 3, 01.09.2004, p. 503-8.

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

Harvard

Pauer, H-U, Renné, T, Hemmerlein, B, Legler, T, Fritzlar, S, Adham, I, Müller-Esterl, W, Emons, G, Sancken, U, Engel, W & Burfeind, P 2004, 'Targeted deletion of murine coagulation factor XII gene-a model for contact phase activation in vivo', THROMB HAEMOSTASIS, vol. 92, no. 3, pp. 503-8. https://doi.org/10.1267/THRO04090503

APA

Pauer, H-U., Renné, T., Hemmerlein, B., Legler, T., Fritzlar, S., Adham, I., Müller-Esterl, W., Emons, G., Sancken, U., Engel, W., & Burfeind, P. (2004). Targeted deletion of murine coagulation factor XII gene-a model for contact phase activation in vivo. THROMB HAEMOSTASIS, 92(3), 503-8. https://doi.org/10.1267/THRO04090503

Vancouver

Pauer H-U, Renné T, Hemmerlein B, Legler T, Fritzlar S, Adham I et al. Targeted deletion of murine coagulation factor XII gene-a model for contact phase activation in vivo. THROMB HAEMOSTASIS. 2004 Sep 1;92(3):503-8. https://doi.org/10.1267/THRO04090503

Bibtex

@article{4e00803a17194e01a01239ba7c8392f6,
title = "Targeted deletion of murine coagulation factor XII gene-a model for contact phase activation in vivo",
abstract = "To analyze the biological role of factor XII (FXII, Hageman Factor) in vivo, we generated mice deficient for FXII using a gene targeting approach on two distinct genetic backgrounds, i.e. mixed C57Bl/6J X 129X1/SvJ and inbred 129X1/SvJ. Homozygous FXII knockout (FXII(-)/(-)) mice showed no FXII plasma activity and had a markedly prolonged activated partial thromboplastin time (aPTT). In contrast, coagulation factors XI, VIII, IX, X,VII, V, II and fibrinogen did not differ between FXII(-/-) mice and their wild-type littermates. Heterozygous matings segregated according to the Mendelian inheritance indicating that FXII deficiency does not increase fetal loss. Furthermore, matings of FXII(-/-) males and FXII(-/-) females resulted in normal litter sizes demonstrating that total FXII deficiency in FXII(-/-) females does not affect pregnancy outcome. Also, gross and histological anatomy of FXII(-/-) mice was indistinguishable from that of their wild-type littermates on both genetic backgrounds. Thus it appears that deficiency of murine FXII does not cause thrombophilia or impaired fibrinolysis in vivo. These results indicate that FXII deficiency does not affect hemostasis in vivo and we anticipate that the FXII(-/-) mice will be helpful to elucidate the biological role(s) of FXII in health and disease.",
keywords = "Animals, Enzyme Activation, Factor XII, Female, Fibrinolysis, Hemostasis, Humans, Inheritance Patterns, Male, Mice, Mice, Knockout, Models, Animal, Partial Thromboplastin Time, Pregnancy, Pregnancy Outcome, Thrombophilia",
author = "Hans-Ulrich Pauer and Thomas Renn{\'e} and Bernhard Hemmerlein and Tobias Legler and Saskia Fritzlar and Ibrahim Adham and Werner M{\"u}ller-Esterl and Guenter Emons and Ulrich Sancken and Wolfgang Engel and Peter Burfeind",
year = "2004",
month = sep,
day = "1",
doi = "10.1267/THRO04090503",
language = "English",
volume = "92",
pages = "503--8",
journal = "THROMB HAEMOSTASIS",
issn = "0340-6245",
publisher = "Schattauer",
number = "3",

}

RIS

TY - JOUR

T1 - Targeted deletion of murine coagulation factor XII gene-a model for contact phase activation in vivo

AU - Pauer, Hans-Ulrich

AU - Renné, Thomas

AU - Hemmerlein, Bernhard

AU - Legler, Tobias

AU - Fritzlar, Saskia

AU - Adham, Ibrahim

AU - Müller-Esterl, Werner

AU - Emons, Guenter

AU - Sancken, Ulrich

AU - Engel, Wolfgang

AU - Burfeind, Peter

PY - 2004/9/1

Y1 - 2004/9/1

N2 - To analyze the biological role of factor XII (FXII, Hageman Factor) in vivo, we generated mice deficient for FXII using a gene targeting approach on two distinct genetic backgrounds, i.e. mixed C57Bl/6J X 129X1/SvJ and inbred 129X1/SvJ. Homozygous FXII knockout (FXII(-)/(-)) mice showed no FXII plasma activity and had a markedly prolonged activated partial thromboplastin time (aPTT). In contrast, coagulation factors XI, VIII, IX, X,VII, V, II and fibrinogen did not differ between FXII(-/-) mice and their wild-type littermates. Heterozygous matings segregated according to the Mendelian inheritance indicating that FXII deficiency does not increase fetal loss. Furthermore, matings of FXII(-/-) males and FXII(-/-) females resulted in normal litter sizes demonstrating that total FXII deficiency in FXII(-/-) females does not affect pregnancy outcome. Also, gross and histological anatomy of FXII(-/-) mice was indistinguishable from that of their wild-type littermates on both genetic backgrounds. Thus it appears that deficiency of murine FXII does not cause thrombophilia or impaired fibrinolysis in vivo. These results indicate that FXII deficiency does not affect hemostasis in vivo and we anticipate that the FXII(-/-) mice will be helpful to elucidate the biological role(s) of FXII in health and disease.

AB - To analyze the biological role of factor XII (FXII, Hageman Factor) in vivo, we generated mice deficient for FXII using a gene targeting approach on two distinct genetic backgrounds, i.e. mixed C57Bl/6J X 129X1/SvJ and inbred 129X1/SvJ. Homozygous FXII knockout (FXII(-)/(-)) mice showed no FXII plasma activity and had a markedly prolonged activated partial thromboplastin time (aPTT). In contrast, coagulation factors XI, VIII, IX, X,VII, V, II and fibrinogen did not differ between FXII(-/-) mice and their wild-type littermates. Heterozygous matings segregated according to the Mendelian inheritance indicating that FXII deficiency does not increase fetal loss. Furthermore, matings of FXII(-/-) males and FXII(-/-) females resulted in normal litter sizes demonstrating that total FXII deficiency in FXII(-/-) females does not affect pregnancy outcome. Also, gross and histological anatomy of FXII(-/-) mice was indistinguishable from that of their wild-type littermates on both genetic backgrounds. Thus it appears that deficiency of murine FXII does not cause thrombophilia or impaired fibrinolysis in vivo. These results indicate that FXII deficiency does not affect hemostasis in vivo and we anticipate that the FXII(-/-) mice will be helpful to elucidate the biological role(s) of FXII in health and disease.

KW - Animals

KW - Enzyme Activation

KW - Factor XII

KW - Female

KW - Fibrinolysis

KW - Hemostasis

KW - Humans

KW - Inheritance Patterns

KW - Male

KW - Mice

KW - Mice, Knockout

KW - Models, Animal

KW - Partial Thromboplastin Time

KW - Pregnancy

KW - Pregnancy Outcome

KW - Thrombophilia

U2 - 10.1267/THRO04090503

DO - 10.1267/THRO04090503

M3 - SCORING: Journal article

C2 - 15351846

VL - 92

SP - 503

EP - 508

JO - THROMB HAEMOSTASIS

JF - THROMB HAEMOSTASIS

SN - 0340-6245

IS - 3

ER -