Figure 4. Role of CHOP in ER stress–induced IICR. (a and b) Macrophages from WT or Chop−/− mice were incubated for 8 h in the absence or presence of 5 µg/ml tunicamycin (TUN; a) or under control (Con) or cholesterol-loading (Chol) conditions (b) and then assayed for IICR (*, P < 0.001; and **, P < 0.05). (c) Macrophages from Chop−/− mice were transduced with adenovirus (Ad) containing murine Ero1a cDNA or a control LacZ construct at 500 MOI. 32 h after the addition of virus, the cells were assayed for IICR. Quantitative data for the post-ATP increment in first peak fmax/f0, including those for control WT mice transduced with adeno-LacZ (which are not displayed on the line-scatter graph), are shown in the right graph (*, P < 0.001). The post-ATP area AUC data also showed restoration of IICR in cholesterol-loaded Chop−/− macrophages by adeno-Ero1a (not depicted). (a–c) Error bars show SEM (n = 3).
Figure 4.

Role of CHOP in ER stress–induced IICR. (a and b) Macrophages from WT or Chop−/− mice were incubated for 8 h in the absence or presence of 5 µg/ml tunicamycin (TUN; a) or under control (Con) or cholesterol-loading (Chol) conditions (b) and then assayed for IICR (*, P < 0.001; and **, P < 0.05). (c) Macrophages from Chop−/− mice were transduced with adenovirus (Ad) containing murine Ero1a cDNA or a control LacZ construct at 500 MOI. 32 h after the addition of virus, the cells were assayed for IICR. Quantitative data for the post-ATP increment in first peak fmax/f0, including those for control WT mice transduced with adeno-LacZ (which are not displayed on the line-scatter graph), are shown in the right graph (*, P < 0.001). The post-ATP area AUC data also showed restoration of IICR in cholesterol-loaded Chop−/− macrophages by adeno-Ero1a (not depicted). (a–c) Error bars show SEM (n = 3).

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