Publikationsansicht

Arg123-Tyr166 domain of human ApoA-I is critical for HDL-mediated inhibition of macrophage homing and early atherosclerosis in mice (2001)

Abstract
Atherosclerosis was studied in apolipoprotein E (apoE) knockout mice expressing human apolipoprotein A-I (apoA-I) or an apoA-I/apolipoprotein A-II (apoA-II) chimera in which the Arg123-Tyr166 central domain of apoA-I was substituted with the Ser12-Ala75 segment of apoA-II. High density lipoprotein (HDL) cholesterol levels were identical in apoA-I and apoA-I/apoA-II mice, but at 4 months, plaques were 2.7-fold larger in the aortic root of the apoA-I/apoA-II mice (P. Center for Experimental Surgery and Anesthesiology, Katholieke Universiteit Leuven, Leuven, Belgium. paul.holvoet@med.kuleuven.ac.be

Details der Publikation
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Keywords Animals, Apolipoprotein A-I, Arteriosclerosis, Autoantibodies, Base Sequence, Cell Adhesion, Chimera, Cholesterol, HDL, Disease Progression, Female, Lipoproteins, HDL, Lipoproteins, LDL, Macrophages, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Oxidative Stress
Typ Description (Metadata) only, IT, article
Sprache Englisch
Verknüpfungen Arteriosclerosis, Thrombosis and Vascular Biology vol:21 issue:12 pages:1977-83