Mechanisms of ER Stress-Mediated Mitochondrial Membrane Permeabilization
Figure 3
Resistance to ER stress-induced death and loss of mitochondrial membrane potential in absence of caspases. (a)–(c) Left panel, Indicated MEFs were treated with (2 M) Tg for 24 hours. Cells were stained with haematoxylin-eosin-stain and visualised using an Olympus IX71 microscope at 40. Images are representative of 2 independent experiments. Right panel, indicated MEFs were treated with (2 M) Tg for the indicated times. Increase in cell death was measured by annexin V staining. The data is representative of at least 2 independent experiments. (d) H9c2 cells were treated with (2 M) Tg alone or pretreated for 30 minutes with Boc-D.fmk (20 M) and DEVD.fmk (20 M) prior to treatment with Tg, for the indicated time periods. Following treatment cells were incubated with (100 nM) TMRE. Mitochondrial membrane potential was monitored by measuring the fluorescence intensity at 582 nm (FL2). As a positive control for depletion of membrane potential, cells were treated with (10 M) CCCP for 45 minutes. The data is a representative of at least three independent experiments. (e)–(f) Indicated MEFs were treated with (2 M) Tg for 24 hours. Following treatment cells were incubated with (100 nM) TMRE. Mitochondrial membrane potential was monitored by measuring the fluorescence intensity at 582 nm (FL2). The data is a representative of at least three independent experiments.
