HIV protease inhibitors promote atherosclerotic lesion formation independent of dyslipidemia by increasing CD36-dependent cholesteryl ester accumulation in macrophages
J. Clin. Invest. James Dressman, et al. 111:389 doi:10.1172/JCI16261 [
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Figure 3Ritonavir does not induce sterol accumulation in peritoneal macrophages isolated from CD36 null mice. Peritoneal macrophages were isolated from the indicated mouse strains and then incubated in the presence of 10% serum and 50 μg/ml of aggregated LDL, along with 30 ng/ml of ritonavir or vehicle (0.01% ethanol) for 24 hours. After the treatment period the cells were lysed, lipids extracted, and processed to quantify total cellular cholesterol and cholesteryl esters by gas chromatography. Bars represent mean ± SE,
n = 3 with triplicate measurements. *
P < 0.01 compared with vehicle.
