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Research Article Free access | 10.1172/JCI117548

Role of the GRO family of chemokines in monocyte adhesion to MM-LDL-stimulated endothelium.

D Schwartz, A Andalibi, L Chaverri-Almada, J A Berliner, T Kirchgessner, Z T Fang, P Tekamp-Olson, A J Lusis, C Gallegos, and A M Fogelman

Department of Medicine, University of California at Los Angeles 90024.

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Department of Medicine, University of California at Los Angeles 90024.

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Department of Medicine, University of California at Los Angeles 90024.

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Department of Medicine, University of California at Los Angeles 90024.

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Department of Medicine, University of California at Los Angeles 90024.

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Department of Medicine, University of California at Los Angeles 90024.

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Department of Medicine, University of California at Los Angeles 90024.

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Department of Medicine, University of California at Los Angeles 90024.

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Department of Medicine, University of California at Los Angeles 90024.

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Published November 1, 1994 - More info

Published in Volume 94, Issue 5 on November 1, 1994
J Clin Invest. 1994;94(5):1968–1973. https://doi.org/10.1172/JCI117548.
© 1994 The American Society for Clinical Investigation
Published November 1, 1994 - Version history
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Abstract

We have previously shown that treatment of endothelial cells with minimally modified LDL (MM-LDL) induces the binding of monocytes to unknown endothelial receptor molecules. We now report that a member of the GRO family of chemokines plays a role in MM-LDL-induced monocyte binding. A cDNA library made from rabbit aortic endothelial cells (RAEC) treated with MM-LDL was expression screened for molecules inducing binding of a human monocyte cell line (THP-1). A cDNA was isolated with 75% homology to GRO. GRO mRNA levels were significantly elevated after exposure of RAEC or human aortic endothelial cells (HAEC) to MM-LDL. HAEC treated with MM-LDL displayed an increase in a surface-associated protein that bound to antibody against GRO despite low levels of GRO in the medium. Antibody to GRO significantly inhibited the binding of monocytes to MM-LDL-treated RAEC and HAEC. The increase in GRO expression and monocyte binding were reduced by incubating MM-LDL-treated endothelial cells with heparin (in a method that releases heparan sulfate bound molecules from the cell surface). These results suggest that GRO related chemokines are bound to the surface of MM-LDL-treated endothelial cells and may contribute to the monocyte adhesion induced by MM-LDL.

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