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 [Go to this article.]

Figure 2
CD36 blocking antibodies and a CD36 morpholino prevent the accumulation of sterol. (a) THP-1 cells were cultured in 100 nM PMA for 72 hours to promote attachment and differentiation of the cells to a macrophage phenotype and then treated with 25 nmol of a CD36 morpholino for 24 hours. The THP-1 cells and CHO cells expressing human CD36 (hCD36) or the vector only were lysed and 20 μg of protein was resolved by SDS-PAGE and immunoblotted with the CD36 blocking antibody. Cross-reactive material was visualized by chemiluminescence. The exposure time was 2 minutes. The data are representative of three independent experiments. (b) THP-1 cells were cultured in 100 nM PMA for 72 hours to promote attachment and differentiation of the cells to a macrophage phenotype. The cells were incubated in the presence of 10% serum and 50 μg/ml of aggregated LDL, along with 30 ng/ml of amprenavir, indinavir, ritonavir, or vehicle (ethanol) for 24 hours. In addition, different sets of cells also contained one of the following: 20 μg/ml of CD36 blocking IgM, 20 μg/ml nonrelevant IgM, or a CD36 morpholino (25 nmol). 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 = 5 with triplicate measurements. *P < 0.01 compared with vehicle, ⁺P < 0.01 compared with amprenavir, ^#P < 0.01 compared with indinavir.