Arterial thrombosis is accelerated in mice deficient in histidine-rich glycoprotein

Author:

Vu Trang T.12,Zhou Ji13,Leslie Beverly A.13,Stafford Alan R.13,Fredenburgh James C.13,Ni Ran12,Qiao Shengjun13,Vaezzadeh Nima12,Jahnen-Dechent Willi4,Monia Brett P.5,Gross Peter L.123,Weitz Jeffrey I.1236

Affiliation:

1. Thrombosis and Atherosclerosis Research Institute,

2. Department of Medical Sciences,

3. Department of Medicine, and

4. Helmholtz-Institute for Biomedical Engineering, Biointerface Laboratory, Rheinisch-Westfälische Technische Hochschule Aachen (RWTH) Aachen University, Aachen, Germany; and

5. Isis Pharmaceuticals, Inc., Carlsbad, CA

6. Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada;

Abstract

Key Points Mice deficient in HRG have normal hemostasis, but demonstrate accelerated thrombosis via the contact system. HRG abrogates nucleic acid–driven coagulation and serves as a novel modulator of the contact system in vivo.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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