1 December 2008
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ISSN 1449-1907

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International Journal of Biological Sciences

Int J Med Sci 2008; 5:240-243 ©Ivyspring International Publisher

Short Research Communication

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

Daniel Chesik, Nadine Wilczak, Jacques De Keyser

Department of Neurology, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, the Netherlands

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.

Keywords: beta adrenergic receptors, insulin-like growth factor, cyclic adenosine monophosphate, astrocytes, multiple sclerosis