We have shown that the stimulation of beta-adrenergic receptors (beta-AR) increases apoptosis in adult @entity35 ventricular myocytes (ARVMs). Integrins, a family of alphabeta-heterodimeric cell surface receptors, are postulated to play a role in ventricular remodeling. Here, we show that @entity1063 (NE) increases beta1 integrins expression in ARVMs via the stimulation of alpha1-AR, not beta-AR. Inhibition of @entity2508 using @entity4286 , an inhibitor of @entity2508 pathway, inhibited alpha1-AR-stimulated increases in beta1 integrins expression. Activation of beta1 integrins signaling pathway using laminin (LN) inhibited beta-AR-stimulated apoptosis as measured by terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL)-staining and flow cytometry. Likewise, ligation of beta1 integrins with anti-beta1 integrin antibodies prevented beta-AR-stimulated apoptosis. Treatment of cells using LN or anti-beta1 integrin antibodies activated @entity2508 pathway. @entity4286 inhibited activation of @entity2508 by LN, and prevented the anti-apoptotic effects of LN. Thus (1) stimulation of alpha1-AR regulates beta1 integrins expression via the activation of @entity2508 , (2) beta1 integrins signaling protects ARVMs from beta-AR-stimulated apoptosis, (3) activation of @entity2508 plays a critical role in the anti-apoptotic effects of beta1-integrin signaling. These data suggest that beta1 integrin signaling protects ARVMs against beta-AR-stimulated apoptosis possibly via the involvement of @entity2508 .

beta1 integrins expression in adult XXXX ventricular myocytes and its role in the regulation of beta-adrenergic receptor-stimulated apoptosis.

@entity35 :: ('10116', 'Species') :: ['rat'] @entity1063 :: ('MESH:D009638', 'Chemical') :: ['norepinephrine'] @entity2508 :: ('50689;116590', 'Gene') :: ['ERK1/2'] @entity4286 :: ('MESH:C093973', 'Chemical') :: ['PD 98059']
@entity35 :: (10116,Species) :: ['rat']
