© 2000 American Heart Association, Inc.
Integrative Physiology |
Reduced Neointima Hyperplasia of Vein Bypass Grafts in Intercellular Adhesion Molecule-1–Deficient Mice
Presented in part at the 72nd Scientific Sessions of the American Heart Association, Atlanta, Ga, November 7–10, 1999, and published in abstract form (Circulation. 1999;100[suppl I]:I-333–I-334).
From the Institute for Biomedical Aging Research (Y.Z., M.M., Q.X.), Austrian Academy of Sciences Innsbruck, Austria; and Institute for General and Experimental Pathology (Y.H., H.D., G.W.), University of Innsbruck Medical School, Innsbruck, Austria.
Correspondence to Dr Qingbo Xu, Institute for Biomedical Aging Research, Austrian Academy of Sciences, Rennweg 10, A-6020 Innsbruck, Austria. E-mail Qingbo.Xu{at}oeaw.ac.at
Abstract—Recently, we established
a new mouse model of vein graft arteriosclerosis
through the grafting of vena cava to carotid arteries. In many
respects, the morphological features of this murine vascular graft
model resemble those of human venous bypass graft disease. With this
model, we studied the role of intercellular adhesion molecule-1
(ICAM-1) in the development of vein graft
arteriosclerosis in ICAM-1–deficient mice.
Neointimal hyperplasia of vein grafts in ICAM-1 -/- mice
was reduced 30% to 50% compared with that of wild-type control
animals. Immmunofluorescent analysis revealed that
increased ICAM-1 expression was observed on the
endothelium and smooth muscle cells (SMCs) of the
grafted veins in wild-type, but not ICAM-1 -/-, mice. MAC-1
(CD11b/18)–positive cells that adhered to the surface of vein grafts
in ICAM-1 -/- mice were significantly less as identified with en face
immunofluorescence, and these positive cells were
more abundant in the intimal lesions of vein grafts in wild-type mice.
Furthermore, aortic SMCs cultivated from wild-type mice exhibited high
ICAM-1 expression in response to tumor necrosis factor-
. When tumor
necrosis factor-–stimulated SMCs were incubated with mouse spleen
leukocytes, the number of cells that adhered to ICAM-1 -/- SMCs was
significantly lower than the number that adhered to ICAM-1 +/+ SMCs,
which was markedly blocked through pretreatment of leukocytes with the
anti–MAC-1 antibody. Taken together, our findings demonstrate that
ICAM-1 is critical in the development of venous bypass graft
arteriosclerosis, which provides essential
information for therapeutic intervention for vein graft disease in
patients undergoing bypass surgery.
Key Words: veins • neointima • adhesion molecules • mice • arteriosclerosis
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