FIG. 3.

Upregulating CD36 increases phagocytosis of RPEs obtained from synchronized cultures. Human monocyte-derived macrophages (mφs) (left side) and BALB/c murine macrophages (right side) were treated with 50 μM troglitazone (□) or with dimethyl sulfoxide as a control (▪) and then used in RPE phagocytosis assays as previously described (21). Fc receptors were blocked in all assays, and where indicated, CD36 was blocked by preincubation with 10 μg of FA6-152 per ml for human macrophages and clone 63 for murine macrophages, or RPEs were pretreated with 50 μg of trypsin per ml and washed before use in phagocytosis assays. Data shown are means ± standard deviations of at least four independent experiments. Phagocytosis of RPEs was increased in macrophages treated with 50 μM troglitazone for 48 h (∼108% ± 31% and 140% ± 33% for human and murine macrophages, respectively) compared to phagocytosis by control macrophages (*, P < 0.01; Student's t test; n = 12 per group). Anti-CD36 and trypsin treatment significantly reduced RPE uptake by troglitazone-treated macrophages (**, P < 0.01).