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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:826.)
© 2007 American Heart Association, Inc.

Vascular Biology

Carbamylated Low-Density Lipoprotein Induces Monocyte Adhesion to Endothelial Cells Through Intercellular Adhesion Molecule-1 and Vascular Cell Adhesion Molecule-1

Eugene O. Apostolov; Sudhir V. Shah; Ercan Ok; Alexei G. Basnakian

From the Division of Nephrology (E.O.A., S.V.S., E.O., A.G.B.), Department of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, Ark; Renal Medicine Service (S.V.S., A.G.B.), Central Arkansas Veterans Healthcare System, Little Rock, Ark; Division of Nephrology (E.O.), Department of Internal Medicine, Ege University Medical School, Izmir, Turkey.

Correspondence to Alexei G. Basnakian, Division of Nephrology, Department of Internal Medicine, University of Arkansas for Medical Sciences, 4301 W. Markham St, Slot 501, Little Rock, AR 72205. E-mail basnakianalexeig{at}uams.edu

Objective— Carbamylated low-density lipoprotein (LDL), the most abundant modified LDL isoform in human blood, has been recently implicated in causing the atherosclerosis-prone injuries to endothelial cells in vitro and atherosclerosis in humans. This study was aimed at testing the hypothesis that carbamylated LDL acts via inducing monocyte adhesion to endothelial cells and determining the adhesion molecules responsible for the recruitment of monocytes.

Methods and Results— Exposure of human coronary artery endothelial cells with carbamylated LDL but not native LDL caused U937 monocyte adhesion and the induction of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 adhesion molecules as measured by cell enzyme-linked immunosorbent assay. Silencing of intercellular adhesion molecule-1 by siRNA or its inhibition using neutralizing antibody resulted in decreased monocyte adhesion to the endothelial cells. Similar silencing or neutralizing of vascular cell adhesion molecule-1 alone did not have an effect but was shown to contribute to intercellular adhesion molecule-1 when tested simultaneously.

Conclusions— Taken together, these data provide evidence that intercellular adhesion molecule-1 in cooperation with vascular cell adhesion molecule-1 are essential for monocyte adhesion by carbamylated low-density lipoprotein-activated human vascular endothelial cells in vitro.

The exposure of human coronary artery endothelial cells with carbamylated LDL but not native LDL caused U937 monocyte adhesion and the induction of ICAM-1 and VCAM-1 adhesion molecules. Silencing of ICAM-1 and VCAM-1 by siRNA or their inhibition using neutralizing antibody resulted in decreased monocyte adhesion to the endothelial cells.

Key Words: atherosclerosis • carbamylated low-density lipoprotein • endothelial cells • intercellular adhesion molecule-1 • monocyte adhesion • vascular cell adhesion molecule-1