Fig. 1
Aβ induced intracellular Ca2+ overload by increasing SOCE, which resulted in ER stress. a Representative blots of GRP78 and CHOP from the hippocampi of postmortem human AD and age-matched controls. b Data are presented as the mean ± SEM (n = 5). The optical density (OD) values of GRP78 and CHOP were normalized to that of β-actin. *p < 0.05 vs. control brains (unpaired, two-tailed Student’s t test). c Representative blots of GRP78 and CHOP from the hippocampi of APP/PS1 mice and age-matched controls. d Data are presented as the mean ± SEM (n = 5). The OD values of GRP78 and CHOP were normalized to that of β-actin. *p < 0.05 vs. control brains (unpaired, two-tailed Student’s t test). e Primary astrocytes were treated with 5 μM Aβ for 6, 12, or 24 h. Then, the cell lysates were subjected to western blot analysis with β-actin as the loading control. f Data are presented as the mean ± SEM (n = 3). The OD values of GRP78 and CHOP were normalized to that of β-actin. *p < 0.05 vs. control cells (unpaired, two-tailed Student’s t test). g Primary cultured astrocytes were treated with 5 μM Aβ for 12 or 24 h and then loaded with the Ca2+ sensitive dye Fluo-4AM at 37 °C for 30 min. Changes in [Ca2+]i were monitored with a FlexStation 3 Multi-Mode Microplate Reader. Fluorescence intensities of [Ca2+]i are shown. Fluorescence intensity was measured in the presence of 1 μM Tg with or without 2 mM Ca2+. Tg thapsigargin. h Quantification (mean ± SEM) of fluorescence intensity. *p < 0.05, **p < 0.01 vs. control cells (one-way ANOVA followed by the Dunnett’s multiple comparison test). i Upregulation of GRP78 in reactive astrocytes of AD patients. Double immunofluorescence staining of GRP78 with GFAP in brain sections of control and AD patients. Nuclei were stained blue with 4′,6-diamidino-2-phenylindole (DAPI). Scale bar: 25 μm