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 Blood, 1 February 2008, Vol. 111, No. 3, pp. 1274-1281.
Prepublished online as a Blood First Edition Paper on November 13, 2007; DOI 10.1182/blood-2007-06-092338.

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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY

Deletion of murine kininogen gene 1 (mKng1) causes loss of plasma kininogen and delays thrombosis

Sergei Merkulov1, Wan-Ming Zhang1, Anton A. Komar2, Alvin H. Schmaier1, Ellen Barnes3, Yihua Zhou1, Xincheng Lu3, Takayuki Iwaki4, Francis J. Castellino4, Guangbin Luo3, and Keith R. McCrae1

1 Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH; 2 Department of Biological, Geological and Environmental Sciences, Cleveland State University, OH; 3 Department of Genetics, Case Western Reserve University School of Medicine, Cleveland, OH; and 4 W. M. Keck Center for Transgene Research, University of Notre Dame, IN

High-molecular-weight kininogen (HK) plays an important role in the assembly of the plasma kallikrein-kinin system. While the human genome contains a single copy of the kininogen gene, 3 copies exist in the rat (1 encoding K-kininogen and 2 encoding T-kininogen). Here, we confirm that the mouse genome contains 2 homologous kininogen genes, mKng1 and mKng2, and demonstrate that these genes are expressed in a tissue-specific manner. To determine the roles of these genes in murine development and physiology, we disrupted mKng1, which is expressed primarily in the liver. mKng1–/– mice were viable, but lacked plasma HK and low-molecular-weight kininogen (LK), as well as {Delta}mHK-D5, a novel kininogen isoform that lacks kininogen domain 5. Moreover, despite normal tail vein bleeding times, mKng1–/– mice displayed a significantly prolonged time to carotid artery occlusion following Rose Bengal administration and laser-induced arterial injury. These results suggest that a single gene, mKng1, is responsible for production of plasma kininogen, and that plasma HK contributes to induced arterial thrombosis in mice.


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