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Fig. 2 | Cell Communication and Signaling

Fig. 2

From: Prion peptide-mediated calcium level alteration governs neuronal cell damage through AMPK-autophagy flux

Fig. 2

PrP (106–126)-mediated increase in the intracellular Ca2+ induced neuronal apoptosis. a SK-N-SH cells were treated with fluo-4 AM and the change in Ca2+ levels was measured using confocal microscopy. The time point of EGTA treatment (2 mM) is shown by the ① arrow and PrP (106–126) treatment (100 μM) is shown by the ② arrow. Data are represented as mean ± SEM. [Ca2+]i was measured at 200 s after the treatment in three independent experiments. b SK-N-SH cells were incubated with EGTA (a calcium chelator) for 1 h and then treated with 100 μM PrP (106–126) for 24 h. Cell viability was evaluated using FITC-annexin V, indicate that EGTA decreased PrP-mediated neurotoxicity. c The bar graph represents the average number of annexin V negative cells. The results represent at least three independent experiments. Data are expressed as the mean ± SEM. * p < 0.05, ** p < 0.01, compared to the PrP-treated group (one-way ANOVA). PrP, Prion peptide (106–126); EGTA, Egtazic acid

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