Peripheral blood mononuclear cells of chronic heart failure (CHF) patients produce great amounts of pro-inflammatory cytokines, indicating that circulating cells are activated and could mirror changes occurring in inflammatory cells infiltrating the failing heart. Adenosine is a regulatory metabolite acting through four membrane receptors that are linked to adenylyl cyclase: activation of the A2A receptor subtype has been reported to inhibit cytokine release. Changes of the adenosinergic system may play a role in CHF development. Here we report an increase of A2A receptor expression, density, and coupling to adenylyl cyclase in blood circulating cells of CHF patients. A2A receptor up-regulation was also found in the explanted hearts of these patients, suggesting that changes of peripheral adenosine receptors mirror changes occurring in the disease target organ. In a cohort of patients followed longitudinally after heart transplantation, alterations of peripheral A2A adenosine receptor progressively normalized to control values within 6 months, suggesting that improvement of cardiac performance is accompanied by progressive restoration of a normal adenosinergic system. These results validate the importance of the A2A receptor in human diseases characterized by a marked inflammatory/immune component and suggest that the evaluation of this receptor in peripheral blood cells may be useful for monitoring hemodynamic changes and the efficacy of pharmacological and non-pharmacological treatments in CHF patients.
|Titolo:||Changes of peripheral A2A adenosine receptors in chronic heart failure and cardiac transplantation.|
|Rivista:||THE FASEB JOURNAL|
|Citazione:||Varani, K., Laghi Pasini, F., Camurri, A., Capecchi, P.l., Maccherini, M., Diciolla, F., et al. (2003). Changes of peripheral A2A adenosine receptors in chronic heart failure and cardiac transplantation. THE FASEB JOURNAL, 17(2), 280-282.|
|Appare nelle tipologie:||1.1 Articolo in rivista|