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Circulation. 2003;108:512-515
Published online before print July 21, 2003, doi: 10.1161/01.CIR.0000085568.13915.1E
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(Circulation. 2003;108:512.)
© 2003 American Heart Association, Inc.

Brief Rapid Communications

Increased Thrombosis After Arterial Injury in Human C-Reactive Protein–Transgenic Mice

Haim D. Danenberg, MD; Alexander J. Szalai, PhD; Rajesh V. Swaminathan, BSc; Lin Peng, MD; Zhiping Chen, MS; Philip Seifert, MS; William P. Fay, MD; Daniel I. Simon, MD; Elazer R. Edelman, MD, PhD

From the Harvard–MIT Division of Health Sciences and Technology, Cambridge, Mass (H.D.D., R.V.S., P.S., D.I.S., E.R.E.); Department of Cardiology, Hadassah University Hospital, Jerusalem, Israel (H.D.D.); Cardiovascular Division, Brigham and Women’s Hospital, Boston, Mass (D.I.S., Z.C., E.R.E.); Division of Clinical Immunology and Rheumatology, The University of Alabama at Birmingham (A.J.S.); and Department of Internal Medicine, University of Michigan Medical School, Ann Arbor (W.P.F., L.P.).

Correspondence to Haim Danenberg, MIT, Bldg 56-322, 77 Massachusetts Ave, Cambridge, MA 02139. E-mail danen{at}mit.edu

Received January 21, 2003; de novo received May 30, 2003; accepted June 16, 2003.

Background— C-reactive protein (CRP), an acute-phase reactant long considered merely an innocent bystander in the inflammatory process, is now recognized as a powerful predictor of cardiovascular events. Emerging in vitro evidence suggests that CRP may have direct proinflammatory and prothrombotic effects on monocytes and endothelial cells. To determine whether CRP directly modulates vascular cell function in vivo, we subjected wild-type mice, which do not express CRP, and human CRP–transgenic (CRPtg) mice to 2 models of arterial injury.

Methods and Results— Baseline serum CRP levels in CRPtg mice were 18±6 mg/L. CRP levels were undetectable in wild-type mice. Transluminal wire injury led to complete thrombotic occlusion of the femoral artery at 28 days in 75% of CRPtg arteries (6 of 8) compared with 17% (2 of 12) in wild-type mice (P<0.05). In a model of arterial photochemical injury, clot formation time was shortened in CRPtg mice; mean time to occlusion was 33±19 minutes compared with 59±19 minutes in wild-type mice (n=10; P<0.05).

Conclusions— Arterial injury in CRPtg mice results in an expedited and higher rate of thrombotic occlusion. This is the first report of a prothrombotic phenotype directly attributable to the presence of human CRP in vivo. Investigation of the inflammatory-thrombotic axis in CRPtg mice may elucidate the prothrombotic actions of CRP in unstable arterial diseases and may pave the way for novel therapeutic interventions for preventing cardiovascular events.


Key Words: inflammation • risk factors • thrombosis • heart disease




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