Adenosine A2a receptor induced gliosis via Akt/NF-kappaB pathway in vitro.

Gliosis is characterized by increased expression of glial fibrillary acidic protein (GFAP) and astroglial proliferation, although the mechanism underlying the process is still largely undefined. This study explores the role of the adenosine A2a receptor (A2aR) in gliosis after ischemia-like injury in a rat astrocyte cell line transfected with A2aR. A2aR transfection enhanced GFAP expression and cell proliferation. A2aR-selective antagonist Sch58261 decreased GFAP expression in a dose- and time-dependent manner with increased activation of Akt, and induced activation of NF-kappaB. An Akt inhibitor reversed the effect of Sch58261. These results suggest that the effect of A2aR on gliosis is related to the Akt/NF-kappaB signal pathway.