International Journal of Cell Biology / 2010 / Article / Fig 1

Research Article

Mechanisms of ER Stress-Mediated Mitochondrial Membrane Permeabilization

Figure 1

ER stress-induced apoptosis in H9c2 cells. (a) H9c2 cells were left untreated or treated with (2  M) Tg, (2  g/ml) Tm or (2  g/ml) BFA for 24 hours. The change in expression levels of ER stress markers was measured by real-time RT-PCR normalizing against GAPDH expression and plotting expression levels relative to the control. Error bars represent mean SD from an experiment performed in duplicate and reproduced twice. (b) H9c2 cells were left untreated or treated with (2  M) Tg for the indicated times. The induction of ER stress markers, Grp78, Grp94 and CHOP was determined by Western blot analysis. β-actin was used to determine equal loading of samples. (c) H9c2 cells were left untreated or treated with (2  M) Tg for the indicated times. After 48 hours of Tg-treatment, cells were stained with haematoxylin-eosin-stain and photographed at 200 magnification. (d) H9c2 cells were left untreated or treated with (2  M) Tg for the indicated times. The processing of procaspase-3 and cleavage of PKCδ were determined by Western blot analysis. The caspase activity was determined using DEVD-AMC. The figure is a representative of three independent experiments.
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