Fig. 5: Compound treatment increases ABCA1-mediated cholesterol efflux in human podocytes.

a Representative ABCA1 and GAPDH Western blots from podocytes treated with Cpd G (left), Cpd A (right), and the LXR agonist Cpd C, at the concentrations indicated (full western blots shown in Supplementary Fig. 4). b apoAI-mediated cholesterol efflux in podocytes treated with Cpd G (left), Cpd A (middle) and Cpd C (right) at the concentrations indicated. Data expressed as the mean ± SD. Treatments with Cpd G or Cpd A were compared to vehicle using one-way ANOVA, followed by Dunnet’s test. P = 0.03 for Cpd G at 10 µM, n = 3, F(3, 8) = 6.9; P = 0.02. for Cpd A, n = 8, F(2, 18) = 3.9; P > 0.05 for other concentrations. Cpd C and vehicle were compared using a two tailed t test: n = 8, t(14) = 4.4, P = 0.0006. c, d Representative western blots for ABCA1, Na⁺/K⁺ ATPase, and ERp72 in plasma membrane (c) and microsomal (d) enriched fractions from podocytes treated with Cpd C (1 µM), Cpd A (5 µM) or Cpd G (10 µM). Full western blots shown in Supplementary Fig. 5. Below, relative ABCA1 quantification normalized to the cellular marker. Samples derived from the same experiment and blots were processed in parallel. Data expressed as the mean ± SD. Treatments compared to vehicle using one-way ANOVA, followed by Dunnett’s test. P = 0.0004, 0.048 and 0.048 for Cpd C, Cpd A, and Cpd G, respectively, in plasma membrane fractions, n = 4, F(3, 12) = 12.3. For microsomal fractions, P < 0.05 only for Cpd C (P = 0.046), n = 3, F(3, 8) = 3.7. e Representative western blot showing OSBPL7 and GAPDH expression from human kidney (K) and podocytes (P). Total proteins from Caco2 (C), HepG2 (H), T (THP1), and HEK293 (H) were also analyzed. Uncropped western blots are shown in Supplementary Fig. 7. f Immunofluorescence staining of mouse kidney cortex showing OSPBL7 (red) expression in glomeruli and tubules. Nuclei stained with DAPI (blue). Synaptopodin (green) was used as a podocyte marker.