Persistent β1-adrenergic stimulation is thought to induce cardiac hypertrophy, alteration in calcium regulation and Cx43 over-expression. Adenosine is a negative feedback inhibitor of adrenergic stimulation in the heart, protecting it from toxic effects of overstimulation. The aim of our study evaluate the effects of adenosine administration on Cx43 and pCx43 expression and [Ca2+]i in Isoproterenol-treatedcardiomiocytesby usingH9c2 cells. Adenosine co-treatment reduced cellular hypertrophy, Cx43, pCx43 and CaMKII over-expression, and reducedintracellularCa2+ overload. These results suggest that the beneficial activity of adenosine on cardiomyocytes underlie the reduction of Cx43-dependent calcium overload and CaMKII over-expression, implying a potential therapeutic in cardiac hypertrophy.
EFFECT OF ADENOSINE ON ISOPROTERENOL-INDUCED HYPERTROPHY IN VITRO. A PRELIMINARY STUDY
POPOLO, Ada;M. Pecoraro;PINTO, Aldo
2014-01-01
Abstract
Persistent β1-adrenergic stimulation is thought to induce cardiac hypertrophy, alteration in calcium regulation and Cx43 over-expression. Adenosine is a negative feedback inhibitor of adrenergic stimulation in the heart, protecting it from toxic effects of overstimulation. The aim of our study evaluate the effects of adenosine administration on Cx43 and pCx43 expression and [Ca2+]i in Isoproterenol-treatedcardiomiocytesby usingH9c2 cells. Adenosine co-treatment reduced cellular hypertrophy, Cx43, pCx43 and CaMKII over-expression, and reducedintracellularCa2+ overload. These results suggest that the beneficial activity of adenosine on cardiomyocytes underlie the reduction of Cx43-dependent calcium overload and CaMKII over-expression, implying a potential therapeutic in cardiac hypertrophy.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
