FIGURE 5.

Absence of liver PCPE2 affects HDL-mediated reverse cholesterol transport and SR-BI expression. A, HDL from diet-fed LDLr^−/− and LDLr^−/−, PCPE2^−/− mice was purified and then radiolabeled with ¹²⁵I as described under “Experimental Procedures.” Approximately 10 × 10⁶ cpm of ¹²⁵I-labeled HDL was retro-orbitally injected into atherogenic diet-fed recipient mice of the indicated genotype. Blood was collected from the contralateral retro-orbital sinus at the indicated times. B, the FCR of ¹²⁵I-labeled HDL were determined from plasma decay curves assuming a one-pool model as described under ”Experimental Procedures.” Data represent the mean ± S.D. of n = 3 mice/group. C, [³H]cholesterol levels in plasma during macrophage reverse cholesterol transport study in LDLr^−/− (gray circles) and LDLr^−/−, PCPE2^−/− (black squares) mice fed an atherogenic diet. Mice were injected intraperitoneally with [³H]cholesterol-labeled J774 foam cells as described under “Experimental Procedures.” D, [³H]cholesterol in feces after 0–48 h collection. The numerical data shown is the mean ± S.D. of n = 5–6 male mice for each genotype. The asterisk indicates statistical significance at p < 0.001. ns, indicates that the difference was not significant. E, an immunoblot analysis of liver SR-BI levels in atherogenic diet-fed mice. F, relative mRNA abundance of liver SR-BI in atherogenic diet-fed mice. Data represent the results from n = 6–10 male mice/genotype. The liver mRNA abundance of SR-BI in LDLr^−/− mouse liver was set at 100%.