Circulating adhesion molecules in apoE-deficient mouse strains with different atherosclerosis susceptibility

Recruitment of inflammatory cells in the arterial wall by vascular adhesion molecules plays a key role in development of atherosclerosis. Apolipoprotein E-deficient (apoE −/−) mice have spontaneous hyperlipidemia and develop all phases of atherosclerotic lesions. We sought to examine plasma levels o...

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Veröffentlicht in:Biochemical and biophysical research communications 2005-04, Vol.329 (3), p.1102-1107
Hauptverfasser: Tian, Jing, Pei, Hong, James, Jessica C., Li, Yuhua, Matsumoto, Alan H., Helm, Gregory A., Shi, Weibin
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Sprache:eng
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Zusammenfassung:Recruitment of inflammatory cells in the arterial wall by vascular adhesion molecules plays a key role in development of atherosclerosis. Apolipoprotein E-deficient (apoE −/−) mice have spontaneous hyperlipidemia and develop all phases of atherosclerotic lesions. We sought to examine plasma levels of soluble vascular cell adhesion molecule-1 (sVCAM-1) and sP-selectin in two apoE −/− strains C57BL/6 (B6) and BALB/c with early or advanced lesions. Mice were fed chow or a Western diet containing 42% fat, 0.15% cholesterol, and 19.5% casein. On either diet, BALB/c.apoE −/− mice developed much smaller atherosclerotic lesions and displayed significantly lower levels of sVCAM-1 and sP-selectin than B6.apoE −/− mice. The Western diet significantly elevated sVCAM-1 levels in both strains and sP-selectin levels in B6.apoE −/− mice. BALB/c.apoE −/− mice exhibited 2-fold higher HDL cholesterol levels on the chow diet and 15-fold higher HDL levels on the Western diet than B6.apoE −/− mice, although the two strains had comparable levels of total cholesterol and triglyceride. Thus, increased atherosclerosis is accompanied by increases in circulating VCAM-1 and P-selectin levels in the two apoE −/− mouse strains, and the high HDL level may protect against atherosclerosis by inhibiting the expression of adhesion molecules in BALB/c.apoE −/− mice.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2005.02.090