Abstract
Aortic valve sclerosis (AVS), an early form of aortic valve disease, develops preferentially on the aortic side of valve leaflets, a predilection that is reflected in an heterogeneous side-specific gene expression profile. It has been ascertained that hypercholesterolemia is sufficient to initiate the endothelial expression of activated leukocyte adhesion molecule (ALCAM; CD166), restricted to the aortic side of the leaflet. Intercellular adhesion molecule-1 (ICAM-1) or vascular cell adhesion molecule-1 (VCAM-1)--both of which are more typically associated with early arterial inflammation--are not differentially expressed. ALCAM up-regulation by hypercholesterolemia suggests a side-specific spatial role in the recruitment of leukocytes to AVS sites.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Activated-Leukocyte Cell Adhesion Molecule / genetics
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Activated-Leukocyte Cell Adhesion Molecule / metabolism*
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Animals
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Aortic Valve / immunology*
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Aortic Valve / pathology
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Endothelial Cells / immunology*
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Endothelial Cells / pathology
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Gene Expression Profiling
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Heart Valve Diseases / genetics
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Heart Valve Diseases / immunology*
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Heart Valve Diseases / pathology
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Hypercholesterolemia / complications*
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Hypercholesterolemia / genetics
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Hypercholesterolemia / immunology
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Hypercholesterolemia / pathology
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Immunohistochemistry
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Inflammation Mediators / metabolism*
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Intercellular Adhesion Molecule-1 / metabolism
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Sclerosis
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Swine
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Up-Regulation
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Vascular Cell Adhesion Molecule-1 / metabolism
Substances
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Activated-Leukocyte Cell Adhesion Molecule
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Inflammation Mediators
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Vascular Cell Adhesion Molecule-1
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Intercellular Adhesion Molecule-1