A2A adenosine receptors are up-regulated in lymphocytes from amyotrophic lateral sclerosis patients. Issue 5 (September 2013)

• Record Type: Journal Article
• Authors: Vincenzi, Fabrizio; Corciulo, Carmen; Targa, Martina; Casetta, Ilaria; Gentile, Mauro; Granieri, Enrico; Borea, Pier Andrea; Popoli, Patrizia; Varani, Katia
• Is Part Of: Amyotrophic lateral sclerosis and frontotemporal degeneration. Volume 14:Issue 5/6(2013)
• Page Start: 406
• Page End: 413
• Publication Date: 2013-09
• Subjects: Adenosine receptors -- ALS patients -- human lymphocytes -- saturation binding experiments -- cyclic AMP assays; 616.839
• DOI: 10.3109/21678421.2013.793358
• Languages: English
• ISSNs: 2167-8421

Abstract

Abstract: Adenosine, a purine nucleoside interacting with A1, A2A, A2B and A3 adenosine receptors (ARs), is a potent endogenous modulator of inflammatory and neuronal processes involved in the pathophysiology of several neurodegenerative diseases. In the present study, ARs were investigated in lymphocytes from patients with amyotrophic lateral sclerosis (ALS) and compared with age-matched healthy subjects. In ALS patients A2A ARs were analysed by using RT-PCR, Western blotting and saturation binding experiments. The effect of A2A AR stimulation on cyclic AMP levels was evaluated in lymphocytes from ALS patients and healthy subjects. An up-regulation of A2A ARs was observed in ALS patients with respect to healthy subjects while A1, A2B and A3 AR affinity and density did not change. In ALS patients, the A2A AR density values correlated with the Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised (ALSFRS-R) scores. Furthermore, the stimulation of A2A ARs mediated a significant increase in cyclic AMP levels in lymphocytes from ALS patients, with a higher potency than in lymphocytes from healthy subjects. In conclusion, the positive correlation between A2A AR density and ALSFRS-R scores could indicate a possible protective effect of this receptor subtype, representing an interesting starting point for the study of alternative therapeutic approaches for ALS based on A2A AR modulation.