Fig. 4: ANKRD1 is increased in GECs in FSGS and contributes to endothelial apoptosis. | Cell Death & Disease

Fig. 4: ANKRD1 is increased in GECs in FSGS and contributes to endothelial apoptosis.

From: Global transcriptomic changes in glomerular endothelial cells in mice with podocyte depletion and glomerulosclerosis

Fig. 4

A Colocalization of ANKRD1 with endothelial marker isolectin GS-IB4 in control and podocyte-depleted diseased mice. Scale bars, 25 μm. B Quantification of glomerular ANKRD1 immunofluorescence intensity (in arbitrary units) in control and diseased mice (n = 6 control mice, n = 7 diseased mice, with at least 30 glomeruli evaluated per mouse). **P < 0.01 between two groups by unpaired two-tailed t-test. C Western blot analysis of cultured GECs expressing short harpin RNA (shRNA) against scrambled control (shScr) or against Ankrd1 (ShAnkrd1-1, -2, -3, -4, and -5, five independent clones) are shown on the left. The densitometric analysis of ANKRD1 normalized to GAPDH is shown for shScr vs. ShAnkrd1-5. D Representative images of cleaved Caspase 3 (cl-Caspase 3) staining in cultured mGECs with or without adriamycin treatment (500 ng/mL) for 24 h. Scale bar, 25 μm. Arrowhead show examples of cl-Caspase 3 positive cells. E Quantification of cl-Caspase 3 positive cells (n = 3 independent experiments, with 20 fields analyzed per group). F Western blot analysis of cl-Caspase 3 in mGECs with or without ADR treatment. Quantification of cl-Caspase 3 levels is shown on the right. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001 between indicated groups by two-way ANOVA with Tukey’s multiple comparison test.

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