Clinical Chemistry
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Clinical Chemistry 55: 1728-1731, 2009. First published July 17, 2009; 10.1373/clinchem.2009.125732
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(Clinical Chemistry. 2009;55:1728-1731.)
© 2009 American Association for Clinical Chemistry, Inc.

Brief Communications

Monomeric C-Reactive Protein Decreases Acetylated LDL Uptake in Human Endothelial Cells

Susanne B. Schwedler1,a, Thomas Hansen-Hagge2, Matthias Reichert1, Daniel Schmiedeke1, Reinhard Schneider1, Jan Galle3, Lawrence A. Potempa4, Christoph Wanner1 and János G. Filep5

1 University of Würzburg, Department of Medicine I, Würzburg, Germany;2 Institute for Microtechnology, Mainz, Germany;3 Klinikum Lüdenscheid, Lüdenscheid, Germany;4 Acphazin Inc., Deerfield, IL, USA;5 Research Center, Maisonneuve-Rosemont Hospital, University of Montréal, Montréal, Canada.

aaddress correspondence to this author at: Department of Medicine I, University Hospital Würzburg, Josef-Schneider-Str. 2, D-97080 Würzburg, Germany. Fax +49-931-201-36502; e-mail pelleas{at}t-online.de.


Abstract

Background: C-reactive protein (CRP) is a risk marker for cardiovascular disease and has been implicated in atherogenesis. In atherosclerotic plaques, it colocalizes with oxidized LDL (oxLDL) and promotes oxLDL uptake by macrophages, suggesting an important cross-talk between CRP and lipid processing. A growing body of evidence indicates the existence of distinct configurations of human CRP, native pentameric (nCRP) and structurally modified monomeric (mCRP), that elicit opposing bioactivities in vitro and in vivo. Here, we tested the impact of mCRP and nCRP on the uptake of acetylated LDL (acLDL), which is internalized by receptors similar to those of oxLDL in human endothelial cells.

Methods: We cultured human umbilical vein endothelial cells (HUVECs) for 8 h with mCRP or nCRP (10–100 mg/L) and measured the uptake of acLDL (10–100 mg/L) over a 20-h period by FACS analysis. To assess the receptors involved, we used function-blocking antibodies against Fc {gamma} receptor CD16 (Fc{gamma}RIII) and CD32 (Fc{gamma}RII), and RT-PCR analysis of CD16, CD32, and the receptor for oxidized LDL (LOX-1). Uptake of acLDL and CRP isoforms was visualized by immunofluorescence.

Results: Culture of HUVECs with mCRP, but not nCRP, decreased uptake of acLDL, which was not prevented by anti-CD16 or anti-CD32 antibodies. LOX-1, CD16, and CD32 were undetectable by RT-PCR. Immunofluorescence showed decreased cytoplasmic acLDL staining in human umbilical vein endothelial cells (HUVECs) treated with mCRP, but not with nCRP.

Conclusions: Monomeric CRP, but not nCRP, decreased acLDL uptake in human endothelial cells independent of CD16, CD32, or LOX-1. Our data support a protective role of mCRP in cardiovascular disease.






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Copyright © 2009 by the American Association for Clinical Chemistry.