Figure 2. Role of ERO1-α in ER stress–induced activation of IICR. (a) Macrophages were transfected with either scrambled RNA (scrRNA) or ERO1-α siRNA, incubated for 8 h in the absence or presence of 5 µg/ml tunicamycin (TUN), and then assayed for IICR. The left graph shows a representative experiment in which Fluo-3 fluorescence is expressed as fmax/f0 as a function of time (the arrow indicates ATP addition). The right bar graphs show the post-ATP area increment in fmax/f0 for the first peak and AUC for the ATP-induced calcium release in the first 40 s for n = 30 cells (*, P < 0.001). (b) The experiment was conducted as in panel a, but the cells were loaded with lipoprotein–cholesterol (Chol) instead being treated with tunicamycin (*, P < 0.01; and **, P < 0.05). (c) The experiment was conducted as in panel b, but the responses in macrophages from WT or Ero1a−/− mice were compared (*, P < 0.001). (a–c) Error bars show SEM.
Figure 2.

Role of ERO1-α in ER stress–induced activation of IICR. (a) Macrophages were transfected with either scrambled RNA (scrRNA) or ERO1-α siRNA, incubated for 8 h in the absence or presence of 5 µg/ml tunicamycin (TUN), and then assayed for IICR. The left graph shows a representative experiment in which Fluo-3 fluorescence is expressed as fmax/f0 as a function of time (the arrow indicates ATP addition). The right bar graphs show the post-ATP area increment in fmax/f0 for the first peak and AUC for the ATP-induced calcium release in the first 40 s for n = 30 cells (*, P < 0.001). (b) The experiment was conducted as in panel a, but the cells were loaded with lipoprotein–cholesterol (Chol) instead being treated with tunicamycin (*, P < 0.01; and **, P < 0.05). (c) The experiment was conducted as in panel b, but the responses in macrophages from WT or Ero1a−/− mice were compared (*, P < 0.001). (a–c) Error bars show SEM.

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