Serotonin induced hypertrophy in cultured adult rat ventricular myocytes, increasing 3H-leucine incorporation by 43% (P<0.001) and total protein content by 22% (P<0.001).
Serotonin induces cardiomyocyte hypertrophy via a novel receptor-independent mechanism requiring hydrogen peroxide production by MAO A and ERK1/2 activation.
p-value: p=<0.001
Reactive oxygen species (ROS) play a critical role in cardiac hypertrophy. We have recently shown that the serotonin-degrading enzyme monoamine oxidase A (MAO A) is an important source of hydrogen peroxide in rat heart. In the present study, we investigated the potential role of hydrogen peroxide generated by MAO A in cardiomyocyte hypertrophy by serotonin. Serotonin (5 microM, 48 h) induced hypertrophy in cultured adult rat ventricular myocytes, as reflected by increased 3H-leucine incorporation (+43%, P80%) prevented by the amine uptake inhibitor imipramine, the MAO inhibitor pargyline and the MEK inhibitor PD 98059. Cardiomyocyte hypertrophy and ERK activation were also inhibited by decreasing intracellular ROS by adenoviral overexpression of catalase or cardiomyocytes treatment with the iron chelator deferoxamine. These data suggest that part of cardiac hypertrophic effect of serotonin requires hydrogen peroxide production by MAO A and ERK1/2 activation. This newly recognized, receptor-independent mechanism of serotonin may contribute to myocardial remodeling and failure.
Bianchi et al. (Wed,) conducted a other in Cardiac hypertrophy. Serotonin was evaluated on Cardiomyocyte hypertrophy (3H-leucine incorporation and total protein content) (p=<0.001). Serotonin induced hypertrophy in cultured adult rat ventricular myocytes, increasing 3H-leucine incorporation by 43% (P<0.001) and total protein content by 22% (P<0.001).
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