© 1998 American Heart Association, Inc.
Original Contributions |
Adhesion of Monocytes to Vascular Cell Adhesion Molecule-1–Transduced Human Endothelial Cells
Implications for Atherogenesis
From the Cardiovascular Research Center and Cardiac Unit (R.E.G., A.R.), Massachusetts General Hospital, Boston; the Vascular Research Division (Y.-C.L., H.T.D., M.A.G., F.W.L.), Department of Pathology, Brigham and Women's Hospital, Boston, Mass; the Department of Medicine and Gladstone Institute of Cardiovascular Disease (D.A.D.), UCSF, San Francisco, Calif; Universidad Complutense (C.C.), Madrid, Spain; Servicio de Inmunologia (F.S.-M.), Hospital de la Princesa, Madrid, Spain; and the Department of Microbiology/Immunology (K.S., G.K.), Northwestern University Medical School, Chicago, Ill.
Correspondence to Dr F.W. Luscinskas, Vascular Research Division, Brigham and Women's Hospital, 221 Longwood Ave, Boston, MA 02115. E-mail fluscinska{at}rics.bwh.harvard.edu
Abstract—To study the role of
vascular cell adhesion molecule-1 (VCAM-1) in monocyte recruitment and
atherogenesis, we constructed a recombinant adenovirus, AdRSVrVCAM-1,
carrying the rabbit VCAM-1 cDNA. We have previously shown that
AdRSVrVCAM-1–transduced human umbilical vein
endothelial cells (HUVECs) support the adhesion of
CD4+ CD45RO+ memory T lymphocytes under laminar
flow conditions. We now demonstrate that AdRSVrVCAM-1–transduced
HUVECs support the adhesion of peripheral blood monocytes
at a shear stress of 
1.5 dyne/cm2. Although VCAM-1
supported only firm adhesion of lymphocytes, it was able to mediate
monocyte rolling, firm adhesion, and transmigration when expressed in
the context of otherwise unactivated vascular
endothelium. VCAM-1–transduced HUVECs supported the
adhesion of as many as 4-fold more monocytes than T cells under laminar
flow. The greater monocyte adhesion was explained at least in part by
leukocyte-leukocyte interactions (secondary adhesions), which were not
seen with T cells. These secondary monocyte interactions were
specifically blocked by monoclonal antibodies to L-selectin and
P-selectin glycoprotein ligand-1. These data demonstrate that VCAM-1
expressed in the context of unactivated vascular
endothelium supports the adhesion of the leukocyte
populations present in atherosclerotic plaque and may contribute to
the predominance of monocytes over lymphocytes.
Key Words: adenovirus • adhesion • atherosclerosis • mononuclear leukocyte
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