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. 2010 Sep;88(9):909-20.
doi: 10.1007/s00109-010-0629-y. Epub 2010 May 8.

Inhibition of foam cell formation using a soluble CD68-Fc fusion protein

Karin Daub  1 , Dorothea Siegel-Axel, Tanja Schönberger, Christoph Leder, Peter Seizer, Karin Müller, Martin Schaller, Sandra Penz, Dagmar Menzel, Berthold Büchele, Andreas Bültmann, Götz Münch, Stephan Lindemann, Thomas Simmet, Meinrad Gawaz
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Inhibition of foam cell formation using a soluble CD68-Fc fusion protein

Karin Daub et al. J Mol Med (Berl). 2010 Sep.

Abstract

The appearance of lipid-rich foam cells is a major feature of vulnerable atherosclerotic plaque formation. The transformation of macrophages into foam cells results from excessive uptake of cholesterol-rich particles by scavenger receptors such as CD68. We cloned a CD68-Fc immunoadhesin, a fusion protein consisting of the extracellular domain of the human CD68 and a human Fc domain, and investigated the function in vitro. Specific binding of CD68-Fc to OxLDL with an affinity of 10 nmol/L was determined by surface plasmon resonance and increased binding to lipid-rich human and ApoE(-/-) mice plaque tissue. This was confirmed both by immunohistochemical staining of CD68-Fc-treated paraffin sections from human plaques and by ELISA-based quantification of CD68-Fc binding to human atherosclerotic plaque extracts. In an in vitro model of macrophage/foam cell formation, CD68-Fc reduced foam cell formation significantly. This was caused both by interference of CD68-Fc with OxLDL uptake into macrophages and platelets and by the inhibition of platelet/OxLDL phagocytosis. Finally, expression of metalloproteinases by macrophages/foam cells was inhibited by CD68-Fc. In conclusion, CD68-Fc seems to be a promising new tool for preventing macrophage/foam cell formation. Thus, CD68-Fc might offer a novel therapeutic strategy for patients with acute coronary syndrome by modulating the generation of vulnerable plaques.

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References

    1. Circulation. 2004 Feb 17;109(6):790-6 - PubMed
    1. Arterioscler Thromb Vasc Biol. 2006 Aug;26(8):1702-11 - PubMed
    1. Nat Clin Pract Cardiovasc Med. 2005 Jun;2(6):309-15 - PubMed
    1. Circulation. 2000 Mar 14;101(10):1091-6 - PubMed
    1. Nat Rev Drug Discov. 2003 Jan;2(1):52-62 - PubMed

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