References
Query Results -- Details
MGI Accession ID: MGI:3653163
J Number: J:111180
Other Accession IDs:
Title: Apolipoprotein AI transgene corrects apolipoprotein E deficiency-induced atherosclerosis in mice.
Authors: Paszty C; Maeda N; Verstuyft J; Rubin EM
Journal: J Clin Invest
Volume: 94
Issue: 2
Date: 1994 Aug
Year: 1994
Pages: 899-903
Review Status: Peer Reviewed
Abstract:
Apolipoprotein E (apo E)-deficient mice are severely hypercholesterolemic and develop advanced atheromas independent of diet. The C57BL/6 strain differs from most inbred strains by having lower HDL concentrations and a high risk of developing early atherosclerotic lesions when fed an atherogenic diet. The relative HDL deficiency and atherosclerosis susceptibility of the C57BL/6 strain are corrected with the expression of a human apolipoprotein AI (apo AI) transgene in this genetic background. To examine if increases in apo AI and HDL are also effective in minimizing apo E deficiency--induced atherosclerosis, we introduced the human apo AI transgene into the hypercholesterolemic apo E knockout background. Similar elevations of total plasma cholesterol occurred in both the apo E knockout and apo E knockout mice also expressing the human apo AI transgene. The latter animals, however, also showed a two- to threefold increase in HDL and a sixfold decrease in susceptibility to atherosclerosis. This study demonstrates that elevating the concentration of apo AI reduces atherosclerosis in apo E deficient-mice and suggests that elevation of apo AI and HDL may prove to be a useful approach for treating unrelated causes of heightened atherosclerosis susceptibility.
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