Key result
Isoproterenol-stimulated ANF expression in rat cardiomyocytes is significantly inhibited by silencing STAT3 or antagonizing gp130 signaling, indicating an essential role for the gp130/STAT3 pathway.
Why the study?
Does gp130/STAT3 signaling mediate beta-adrenergic receptor-induced ANF expression in rat cardiomyocytes?
Does gp130/STAT3 signaling mediate beta-adrenergic receptor-induced ANF expression in rat cardiomyocytes?
The study demonstrates that gp130/STAT3 signaling plays an essential role in beta-adrenergic receptor-induced ANF expression in cardiomyocytes, providing insight into the molecular mechanisms of cardiac remodeling.
Supports mechanistic studies of beta-adrenergic remodeling; leaves open clinical relevance of gp130/STAT3 in human heart failure.
beta-Adrenergic receptor (beta-AR)-induced cardiac remodeling is closely linked with the re-expression of the atrial natriuretic factor (ANF) gene. However, the exact molecular mechanism of this response remains elusive. Here, we demonstrate that the beta-AR agonist isoproterenol potently evokes the tyrosine phosphorylation of STAT3 and increases its transcriptional activity in an extracellularly regulated kinase 1/2 and glycoprotein (gp)130 signaling-dependent manner in rat cardiomyocytes. Interestingly, both specific silencing of signal transducers and activators of transcription 3 (STAT3) expression by lentivirus-mediated RNA interference and antagonism of gp130 signaling lead to significant inhibition of isoproterenol-stimulated ANF expression. Together, these results indicate that gp130/STAT3 signaling has an essential role in ANF expression by beta-AR stimulation.
No takes yet. Share an insight, caveat, or question.
Zhang et al. (2008) studied Cardiac remodeling. Isoproterenol, STAT3 silencing, and gp130 antagonism was evaluated on Atrial natriuretic factor (ANF) expression and STAT3 phosphorylation. Isoproterenol-stimulated ANF expression in rat cardiomyocytes is significantly inhibited by silencing STAT3 or antagonizing gp130 signaling, indicating an essential role for the gp130/STAT3 pathway.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: