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 6
HIV protease inhibitors induce an increase of CD36 protein levels in peritoneal macrophages. Six-week-old male LDLR null mice on a chow diet were given vehicle control (0.01% ethanol) or the following protease inhibitors in their drinking water: amprenavir (23 or 75 μg/mouse/day), indinavir (25 or 75 μg/mouse/day), or ritonavir (10 or 50 μg/mouse/day). (a) After 8 weeks of treatment, peritoneal macrophages were isolated, the cells were lysed, and 20 μg of protein was resolved by SDS-PAGE and immunoblotted with antibodies for CD36, SRA, and actin. The data are representative of eight mice. (b) After 8 weeks of treatment, cardiac myocytes (38), adipocytes (39), and platelets (40) were isolated, the cells were lysed, and 20 μg of protein was resolved by SDS-PAGE and immunoblotted with antibodies against CD36. The data are representative of eight mice.