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C-Reactive Protein and Complement Are Important Mediators of Tissue Damage in Acute Myocardial Infarction

C-Reactive Protein and Complement Are Important Mediators of Tissue Damage in Acute Myocardial... Myocardial infarction in humans provokes an acute phase response, and C-reactive protein (CRP), the classical acute phase plasma protein, is deposited together with complement within the infarct. The peak plasma CRP value is strongly associated with postinfarct morbidity and mortality. Human CRP binds to damaged cells and activates complement, but rat CRP does not activate complement. Here we show that injection of human CRP into rats after ligation of the coronary artery reproducibly enhanced infarct size by ∼40%. In vivo complement depletion, produced by cobra venom factor, completely abrogated this effect. Complement depletion also markedly reduced infarct size, even when initiated up to 2 h after coronary ligation. These observations demonstrate that human CRP and complement activation are major mediators of ischemic myocardial injury and identify them as therapeutic targets in coronary heart disease. heart ischemia necrosis inflammation acute phase response Footnotes Abbreviations used in this paper: CRP, C-reactive protein; NBT, nitroblue tetrazolium; SAP, serum amyloid P component. Submitted: 14 July 1999 Revision requested 4 October 1999 Accepted: 8 October 1999 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Experimental Medicine Rockefeller University Press

C-Reactive Protein and Complement Are Important Mediators of Tissue Damage in Acute Myocardial Infarction

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References (47)

Publisher
Rockefeller University Press
Copyright
© 1999 The Rockefeller University Press
ISSN
0022-1007
eISSN
1540-9538
DOI
10.1084/jem.190.12.1733
Publisher site
See Article on Publisher Site

Abstract

Myocardial infarction in humans provokes an acute phase response, and C-reactive protein (CRP), the classical acute phase plasma protein, is deposited together with complement within the infarct. The peak plasma CRP value is strongly associated with postinfarct morbidity and mortality. Human CRP binds to damaged cells and activates complement, but rat CRP does not activate complement. Here we show that injection of human CRP into rats after ligation of the coronary artery reproducibly enhanced infarct size by ∼40%. In vivo complement depletion, produced by cobra venom factor, completely abrogated this effect. Complement depletion also markedly reduced infarct size, even when initiated up to 2 h after coronary ligation. These observations demonstrate that human CRP and complement activation are major mediators of ischemic myocardial injury and identify them as therapeutic targets in coronary heart disease. heart ischemia necrosis inflammation acute phase response Footnotes Abbreviations used in this paper: CRP, C-reactive protein; NBT, nitroblue tetrazolium; SAP, serum amyloid P component. Submitted: 14 July 1999 Revision requested 4 October 1999 Accepted: 8 October 1999

Journal

The Journal of Experimental Medicine – Rockefeller University Press

Published: Dec 20, 1999

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