Activation of catalase by apelin prevents oxidative stress-linked cardiac hypertrophy.

Camille Foussal (1) , Olivier Lairez (1) , Denis Calise (2) , Atul Pathak (1) , Céline Guilbeau-Frugier (3) , Philippe Valet (1) , Angelo Parini (1) , Oksana Kunduzova (1)

1 I2MR - Institut de médecine moléculaire de Rangueil
2 Service de Microchirurgie Expérimentale
3 Service d'anatomie pathologique et histologie-cytologie [Rangueil]

Adipose tissue secretes a variety of bioactive factors, which can regulate cardiomyocyte hypertrophy via reactive oxygen species (ROS). In the present study we investigated whether apelin affects ROS-dependent cardiac hypertrophy. In cardiomyocytes apelin inhibited the hypertrophic response to 5-HT and oxidative stress induced by 5-HT- or H(2)O(2) in a dose-dependent manner. These effects were concomitant to the increase in mRNA expression and activity of catalase. Chronic treatment of mice with apelin attenuated pressure-overload-induced left ventricular hypertrophy. The prevention of hypertrophy by apelin was associated with increased myocardial catalase activity and decreased plasma lipid hydroperoxide, as an index of oxidative stress. These results show that apelin behaves as a catalase activator and prevents cardiac ROS-dependent hypertrophy.

Domaines: Biochimie, Biologie Moléculaire

Camille Foussal, Olivier Lairez, Denis Calise, Atul Pathak, Céline Guilbeau-Frugier, et al.. Activation of catalase by apelin prevents oxidative stress-linked cardiac hypertrophy.. FEBS Letters, 2010, 584 (11), pp.2363-70. ⟨10.1016/j.febslet.2010.04.025⟩. ⟨inserm-00505022⟩