Figure 2.

The mutant ARC, unphosphorylated at the 149th position, unable to inhibit the ET 1–induced cardiomyocyte hypertrophy and endogenous sensitization with ARC by applying its sense strand. A: Cultured neonatal rat cardiomyocytes were infected for 24 hr with different “moi” of adenovirus ARC (ARC), nonphosphorylated mutant (T149A), or viral control (Adβ-gal). After infection, they were stimulated for 24 hr with 0.1 μM ET-1. The cell-surface area was analyzed by measuring 200 cells in 40 to 50 fields. The data indicated are mean ± SEM of 3 independent experiments. *P < 0.05, vs ET-1 alone and ET-1 in presence of viral control, ‡P > 0.05, vs ET-1 alone and ET-1 in presence of viral control. Photographs of cultured neonatal rat cardiomyocytes were obtained at 100x resolution, bar = 600 pixels; B: control; C: 24 hr after applying ET 1–induced hypertrophic stimuli; D: CMC treatment with 100 moi AdARC, followed by 24 hr ET-1 stimuli; E: CMC treatment with nonphosphorylated ARC mutant T149 A, followed by ET-1 stimuli