Catestatin reverses the hypertrophic effects of norepinephrine in H9c2 cardiac myoblasts by modulating the adrenergic signaling.

摘要: Catestatin (CST) is a catecholamine release-inhibitory peptide secreted from the adrenergic neurons and adrenal glands. It regulates cardiovascular functions it associated with diseases. Though its mechanisms of actions are not known, there evidences cross-talk between CST signaling. We hypothesized that moderates overdrive studied effects on norepinephrine-mediated hypertrophic responses in H9c2 cardiac myoblasts. alone regulated expression number fetal genes induced during hypertrophy. When cells were pre-treated CST, blunted modulation those by norepinephrine. Norepinephrine (2 µM) treatment also increased cell size enhanced level Troponin T sarcomere. These attenuated CST. immediate generation ROS increase glutathione peroxidase activity norepinephrine treatment. Expression fosB AP-1 promoter–reporter constructs was used as endpoint readout for interaction signals at gene level. showed largely attenuates stimulatory other mitogenic through regulatory modules characteristic manner. Depending upon dose, signaling appears to be disparate, 10–25 nM doses, primarily moderated β1/2-adrenoceptors. This study, first time, provides insights into heart