Int J Med Sci 2008; 5(5):240-243. doi:10.7150/ijms.5.240
Short Research Communication
IGF-1 regulates cAMP levels in astrocytes through a β2-adrenergic receptor-dependant mechanism
Department of Neurology, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, the Netherlands
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
Chesik D, Wilczak N, De Keyser J. IGF-1 regulates cAMP levels in astrocytes through a β2-adrenergic receptor-dependant mechanism. Int J Med Sci 2008; 5(5):240-243. doi:10.7150/ijms.5.240. Available from http://www.medsci.org/v05p0240.htm