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β3-adrenoceptor(β3-AR) has been shown to promote myocardial apoptosis. However, the exact physiological role and importance of this receptor in the human myocardium, and its underlying mode of action, have not been fully elucidated. The present study aimed to determine the effects of β3-AR on the promotion of myocardial apoptosis and on norepinephrine(NE) injury. We analyzed NE-induced cardiomyocyte(CM) apoptosis by using a TUNEL and an annexin V/propidium iodide apoptosis assay. Furthermore, we investigated the NE-induced expression of the apoptosis marker genes Akt and p38 MAPK, their phosphorylated counterparts p-Akt and p-p38 MAPK, caspase-3, Bcl-2, and Bax. In addition, we determined the effect of a 48-h treatment with a β3-AR agonist and antagonist on expression of these marker genes. β3-AR overexpression was found to increase CM apoptosis, accompanied by an increased expression of caspase-3, bax/bcl-2, and p-p38 MAPK. In contrast, the β3-blocker reduced apoptosis of CMs and the associated elevated Akt expression. We identified a novel and potent anti-apoptosis mechanism via the PI3K/Akt pathway and a pro-apoptosis pathway mediated by p38 MAPK.
However, the exact physiological role and importance of this receptor in the human myocardium, and its underlying mode of action, have not been fully elucidated. The present study aimed to determine the effects of β3-AR on the promotion of myocardial apoptosis and on norepinephrine (NE) injury. We, the NE-induced cardiomyocyte (CM) apoptosis by using a TUNEL and an annexin V / propidium iodide apoptosis assay. NE-induced expression of the apoptosis marker genes Akt and p38 MAPK, their phosphorylated counterparts p-Akt and p-p38 MAPK, caspase-3, Bcl-2, and Bax. with a β3-AR agonist and antagonist on expression of these marker genes. β3-AR overexpression was found to increase CM apoptosis, accompanied by an increased expression of caspase-3, bax / bcl-2, and p-p38 MAPK. , the β3-blocker reduced apoptosis of CMs an d the associated elevated Akt expression. We identified a novel and potent anti-apoptosis mechanism via the PI3K / Akt pathway and a pro-apoptosis pathway mediated by p38 MAPK.