IGF-1 regulates cAMP levels in astrocytes through a β2- adrenergic receptor-dependant mechanism

Abstract

We have recently demonstrated that neonatal astrocytes derived from mice lacking beta-2 adrenergic receptors (β2AR) possess higher proliferation rates, as compared to wild-type cells, an attribute that was shown to involve insulin-like growth factor (IGF) signaling. In the present study, we demonstrate that basal cAMP levels in β2AR knockout astrocytes were significantly lower than in wild type cells. Furthermore, treatment with IGF-1 reduced intracellular cAMP levels in wild type astrocytes, yet had no effects on cAMP levels in β2AR deficient astrocytes. Our data suggests that IGF-1 treatment influences cAMP production through a β2AR-dependant mechanism in astrocytes. A deficit of β2AR on astrocytes, as previously reported in multiple sclerosis, may influence cell proliferation, an action which could have implications in processes involved in astrogliosis. © Ivyspring International Publisher. All rights reserved.