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. 2019 Jun 24;116(28):14154–14163. doi: 10.1073/pnas.1813580116

Fig. 5.

Fig. 5.

K201 attenuates ER calcium release, downstream calpain 2-caspase 12 activation, and apoptosis in Tg-C321R podocytes. Cultured primary podocytes from Tg-WT and Tg-C321R mice at P27 were treated with 5 μM K201 or DMSO (vehicle control) for 24 h. (A) Cytosolic calcium levels in DMSO- and K201-treated podocytes were measured by the cytosolic calcium indicator Fluo-4. Mean ± SD of 3 independent experiments. ***P < 0.001 by ANOVA. Podocyte lysates treated with or without K201 were analyzed by WB for levels of phospho-RyR2 (p-RyR2; Ser2808) and RyR (B), cleaved spectrin and talin 1 (C), and cleaved caspase 12 and caspase 3 (D). Arrows indicate cleaved proteins. (E) Podocyte early apoptotic rate in the presence or absence of K201 was assessed by flow cytometry analysis of Annexin V+/PI− podocytes. The percentage of early apoptotic cells was expressed as mean ± SD from 3 independent experiments. PE, phycoerythrin. *P < 0.05 by ANOVA. NS, not significant by ANOVA.