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Hypolipidemic and hyperlipidemic phenotypes in transgenic mice expressing human apolipoprotein E2
Y Huang1, S W Schwendner, S C Rall
1Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, California 94141-9100, USA.
The Journal of Biological Chemistry
|November 15, 1996
Summary
Transgenic mice expressing human apolipoprotein E2 (apoE2) showed varied lipid profiles. High apoE2 levels caused hyperlipidemia, while intermediate levels led to hypolipidemia, creating a model for type III hyperlipoproteinemia.
Area of Science:
- Lipid Metabolism
- Genetics
- Cardiovascular Disease Research
Background:
- Human apolipoprotein E2 (apoE2) is linked to type III hyperlipoproteinemia (HLP).
- Understanding apoE2's role in lipid regulation is crucial for HLP research.
Purpose of the Study:
- To create and characterize transgenic mouse models expressing varying levels of human apoE2.
- To investigate the impact of different apoE2 plasma concentrations on lipid phenotypes.
- To develop an animal model that mimics human type III HLP.
Main Methods:
- Generation of transgenic mice expressing human apoE2 at different plasma levels.
- Cross-breeding apoE2 transgenic mice with apoB transgenic mice.
- Analysis of lipid profiles (cholesterol, VLDL, IDL, LDL) and lipoprotein characteristics.
Main Results:
- Low apoE2 levels (<10 mg/dl) had minimal effect on lipid phenotype.
- Intermediate apoE2 levels (10-30 mg/dl) resulted in hypolipidemia, primarily reduced HDL cholesterol.
- High apoE2 levels (>50 mg/dl) induced hyperlipidemia with increased VLDL and IDL, resembling type III HLP. Double transgenics (apoE2/apoB) also showed a type III HLP phenotype.
Conclusions:
- Plasma apoE2 levels dictate a hypolipidemic or hyperlipidemic phenotype in transgenic mice.
- This model allows for studying factors influencing hypolipidemia and type III HLP.
- Lipoprotein characteristics, including electrophoretic mobility, are altered by apoE2 expression.