(Hypertension. 1995;25:511-516.)
© 1995 American Heart Association, Inc.
Articles |
Low-Density Lipoprotein Induces Vascular Adhesion Molecule Expression on Human Endothelial Cells
From the Franz Volhard Clinic and the Max-Delbrück Center for Molecular Medicine, University Hospitals Rudolf Virchow (H.H., D.S., W.Z., F.C.L.), the Department of Medicine-Nephrology, Klinikum Steglitz University Hospital (H.H., S.P., A.D.), and the Department of Biochemistry, Free University (M.K.), Berlin, Germany.
Correspondence to Hermann Haller, MD, Franz Volhard Klinik, Wiltberg Strasse 50, 13122 Berlin, Germany.
Abstract We tested the hypothesis that low-density
lipoprotein (LDL) and its acetylated form influence surface expression
of vascular adhesion molecules on human endothelial cells. Vascular
adhesion molecule surface expression was assessed with flow cytometry
on cultured endothelial cells with a modified enzyme-linked
immunosorbent assay. LDL acetylation was determined by chromatography.
Monocyte adhesion to endothelial cells was assessed with U937 cells by
direct counting. Tumor necrosis factor-
(10 ng/mL), a positive
control, induced a time-dependent expression of vascular adhesion
molecules (P<.05), which peaked at 5 hours. Incubation of
endothelial cells with LDL (1.3 to 26.0 mmol/L) led to an increase in
expression at 2 and 5 hours (P<.05). Prolonged (24-hour)
exposure to LDL resulted in a second peak. The effect of acetylated LDL
on expression was not different from that of native LDL. Incubation
with the protein kinase C inhibitor staurosporine (5x10-8
mol/L) blocked the effects of both native and acetylated LDL completely
(P<.05). The calcium channel blocker nitrendipine
(10-7 mol/L) did not influence the expression of vascular
adhesion molecule at 2 and 5 hours but did reduce the effect of LDL on
expression at 24 hours. LDL (2.6 mmol/L) also induced a significant
increase in the surface expression of intercellular adhesion molecule-1
but did not affect the expression of endothelial adhesion molecules.
LDL (2.6 mmol/L) induced a significant increase in monocyte binding. We
conclude that LDL can induce the expression of vascular adhesion
molecules on endothelial cells. This effect is mediated by protein
kinase C and partially inhibited by calcium channel blockade. Our
results suggest that LDL may increase the recruitment of monocytes
through a protein kinase C–mediated increase in adhesion molecule
surface expression.
Key Words: cell adhesion molecules • endothelium • lipoproteins, LDL • protein kinase C • calcium channel blockers
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