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 9Ritonavir increases CD36 and PPAR-γ mRNA in a PKC-dependent manner. Human PBMCs were incubated in the presence of 10% serum and 50 μg/ml aggregated LDL (agLDL) and/or 30 ng/ml ritonavir as indicated for 24 hours. In addition, some sets of cells were also treated with PMA (100 nM), (diacylglycerol [DAG]; 20 μM), Go6976 (500 nM), calphostin C (200 nM), 15d-PGJ2 (1 μM), or ciglitazone (13 μM). The cells were then lysed, mRNA was isolated, and the relative amounts of CD36, PPAR-γ, and GAPDH mRNA were determined by Northern analysis. Shown are representative data from three independent experiments.
