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Fig. 3 | Journal of Biomedical Science

Fig. 3

From: Tetrandrine ameliorates cognitive deficits and mitigates tau aggregation in cell and animal models of tauopathies

Fig. 3

Pathological tau disrupts lysosomal Ca2+ and pH homeostasis by increasing TPC2 activity. A Left, a diagram depicts the topological representation of transfected GCaMP6m-TPC2 in the lysosome. Ca2+-sensitive GCaMP6 is located on the cytoplasmic side and can sense Ca2+ released from lysosomes. Middle, representative Ca2+ traces showing lysosome Ca2+ efflux measured by the expressed GCaMP6m-TPC2 in WT or mutant tau-expressing SH-SY5Y cells. The bar chart on the right shows the normalized peak fluorescence intensity (F/F0) of GCaMP6m-TPC2, summarized as the mean ± SEM from 3 individual experiments, with 90 cells analysed in each group. B Representative Ca2+ traces depict the changes in cytoplasmic Ca2+ content measured by the Ca2+ indicator Fura-2AM after the addition of GPN to SHSY5Y cells expressing Tau-WT or Tau-P301L with or without tetrandrine treatment. Each trace summarizes the changes in cytoplasmic Ca2+ in 90 cells from 3 experiments. The bar chart on the right shows the peaks of GPN-induced cytoplasmic Ca2+ changes. C Lysosomal pH measurements of SH-SY5Y cells expressing Tau-WT or Tau-P301L. The V-ATPase inhibitor bafilomycin A1 (BafA1) was used as a control. D Lysosomal cathepsin D (Cat D) activity measured in SH-SY5Y cells expressing Tau-WT or Tau-P301L. BafA1 was used as a control. Unless otherwise specified, all data are summarized as the mean ± SEM from at least 3 individual experiments; *Indicates p < 0.05

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