Multiple Metabolic Hits Converge on CD36 as Novel Mediator of Tubular Epithelial Apoptosis in Diabetic Nephropathy (original) (raw)
Figure 4
AGE-BSA, CML-BSA, and FFA PA Induce Apoptosis in Human PTECs through CD36 Signaling
Bar graphs show mean ± SEM of apoptotic nuclei, visualized by DAPI staining and normalized to 100 total cells, in human HK-2 PTECs. Data are derived from three independent repeat experiments. Numbers on top of bars indicate significant _p_-values of experimental groups relative to control, or as indicated by bracket.
(A) Cells were treated for 48 h with control BSA (40 μM), TSP-1 (1 μg/ml), and AGE-BSA modified for 2, 5, or 10 weeks (AGE-BSA2, AGE-BSA5, and AGE-BSA10, respectively) in the absence or presence of control IgG (10 μg/ml) or anti-CD36 neutralizing antibody (10 μg/ml), as indicated.
(B) Cells were treated with control BSA (40 μM), or CMLmin-BSA at 0.5, 1, 2, 5, and 10 μM, in the absence or presence of anti-CD36 neutralizing antibody, as indicated.
(C) Cells were treated with monounsaturated FFA oleic acid (OA) or PA at increasing concentrations, in the absence or presence of control IgG (10 μg/ml) or anti-CD36 neutralizing antibody (10 μg/ml), as indicated.