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. Author manuscript; available in PMC: 2009 May 8.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2009 Jan 22;29(4):539–547. doi: 10.1161/ATVBAHA.108.179937

Figure 3.

Figure 3

Increased ApoA1-HDL secretion by hepatocytes from high-cholesterol diet-fed LDLR-/-G2A-/- mice. A (left), FPLC separation of lipoproteins secreted into culture medium over 18 hours by freshly isolated hepatocytes from high-cholesterol diet-fed (20 weeks) LDLR-/-G2A+/+ and LDLR-/-G2A-/- mice. Inset, Immunoblot of HDL fractions showing significant increases in ApoA1 and ApoE in HDL fractions secreted by LDLR-/-G2A-/- hepatocytes. Anti-ApoE immunoblot of VLDL/LDL fractions shown alongside. Right, Densitometric quantification of ApoA1 and ApoE immunoreactivity and total phospholipid content in the indicated HDL fractions. Data shown is representative of 3 independent experiments. B, Quantitative RT-PCR analysis of the expression of the indicated genes in primary hepatocytes and macrophages from male high-cholesterol diet-fed (20 weeks) LDLR-/-G2A+/+ and LDLR-/-G2A-/- mice. The data shown are the average of 3 independent experiments, each performed in triplicate. C, Immunoblot analysis of ApoA1, ApoE, and ABCA1 levels in primary hepatocytes from high-cholesterol diet-fed (20 weeks) LDLR-/-G2A+/+ and LDLR-/-G2A-/- mice (1: LDLR-/-G2A+/+, 2: LDLR-/-G2A-/-). Macrophage ApoE levels in the same mice shown alongside.