Fig. 4: The changes of [Ca2+]i and intracellular signaling in podocytes exposed to cinacalcet and high-glucose media. | Cell Death & Disease

Fig. 4: The changes of [Ca2+]i and intracellular signaling in podocytes exposed to cinacalcet and high-glucose media.

From: Cinacalcet-mediated activation of the CaMKKβ-LKB1-AMPK pathway attenuates diabetic nephropathy in db/db mice by modulation of apoptosis and autophagy

Fig. 4

a The changes of [Ca2+]i in podocytes exposed to cinacalcet and high-glucose media. To determine whether the addition of cinacalcet might modulate [Ca2+]i in podocytes, FURA-2AM-loaded podocytes were stimulated using different concentrations (15, 100 nM) of cinacalcet in low-glucose (LG; 5 mmol/l D-glucose) or high-glucose (HG; 30 mmol/l D-glucose) media. The AUC was estimated from the baseline of normalized data (at the point of injection) to a fluorescence level and between time points of injection (0 min) and 10 min. The peak of the curve was measured as highest value of the curve. The peak amplitude and AUC of [Ca2+]i were significantly increased by cinacalcet in dose-dependent manners in both LG and HG media. In Fig. 4a, the arrow denotes the administration of cinacalcet (15 and 100 nM, respectively) (n = 6 independent experiments in each experiments). **P < 0.01 compared with LG and HG and *P < 0.05 compared with LG + 15 and HG + 15. b The changes of intracellular signaling in podocytes exposed to cinacalcet and high-glucose media. Representative immunofluorescent (n = 6 independent experiments in each experiments) and western blot analyses (n = 4 independent experiments in each experiments) of CaSR, CaMKKβ, phosphor-Ser428 LKB1, and phospho-Thr172 AMPK in the cultured podocytes in low-glucose (LG; 5 mmol/l D-glucose) or high-glucose (HG; 30 mmol/l D-glucose) conditions with or without cinacalcet treatment (15 nM) and the quantitative analyses of the results are shown (n = 6 independent experiments in each experiments). *P < 0.05; **P < 0.01 and #P < 0.001 compared with other groups

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