Rotigaptide (100 nM) increased Cx43 protein expression in neonatal rat ventricular cardiomyocytes, partially reversing cycloheximide-induced reductions (56% vs 39% of vehicle).
Does rotigaptide increase Connexin 43 protein expression in neonatal rat ventricular cardiomyocytes?
Rotigaptide increases Connexin 43 protein expression in neonatal rat ventricular cardiomyocytes, partly through increased biosynthesis.
Absolute Event Rate: 56% vs 39%
Rotigaptide (formerly ZP123) is a novel antiarrhythmic peptide that prevents uncoupling of connexin 43 (Cx43)-mediated, gap junction communication during acute metabolic stress. Since rotigaptide's long-term effects on Cx43 are unknown, we studied its effect on Cx43 protein levels at 24 h in neonatal ventricular myocytes. As determined by Western blot analysis, rotigaptide produced a dose-dependent increase in Cx43 protein expression that reached a maximum level at 100 nM. Furthermore, 100 nM rotigaptide markedly increased Cx43 immunoreactivity and Cx43-positive gap junctions as observed in immunocytochemical studies. Cycloheximide, an inhibitor of protein synthesis, was used to investigate rotigaptide's mechanism of action. Cycloheximide (10 microg/ml) reduced Cx43 protein levels to 39% of vehicle (17 mM ethanol) whereas cotreatment of 10 microg/ml cycloheximide with 100 nM rotigaptide reduced Cx43 protein levels to 56% of vehicle. Our findings suggest that rotigaptide's effect on Cx43 expression is partly due to increased biosynthesis.
Stahlhut et al. (Sun,) reported a other. Rotigaptide (ZP123) vs. Vehicle (17 mM ethanol) was evaluated on Cx43 protein levels. Rotigaptide (100 nM) increased Cx43 protein expression in neonatal rat ventricular cardiomyocytes, partially reversing cycloheximide-induced reductions (56% vs 39% of vehicle).
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