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. 2013 Aug;16(8):928–935.

Figure 3.

Figure 3

Inhibition of endogenous ARC phosphorylation sensitizes cardiomyocytes to undergo ET-1 induced hypertrophy. A: ARC antisense (ARC-AS), scrambled ARC antisense (S-ARC-AS) and ARC sense strands (ARC-S) treated cardiomyocytes were stimulated with Et-1 (5nM). Fold increase in total protein level was analyzed by [3H] Leucine incorporation method. B: Western Blot confirming ARC anti sense (ARC-AS) strand inhibited endogenous ARC production, Lane 2. The cultured neonatal rat cardiomyocytes were incubated with different doses of CK2 inhibitors. C: treatment with DRB to check its dose-dependent effect; 24 hr after incubation with different doses of DRB (25, 50, and 75μM), cells were stimulated with 0.01 μM ET-1. Cell-surface area was measured and data are expressed as the mean ± SEM of 3 independent experiments; *P < 0.05, vs 0.01 μM ET-1. D: TBB group–0.2, 1, and 5 M TBB (50 min incubation)–treated group; *P < 0.05, vs ET-1. The data indicate mean ± SEM of 3 independent experiments