Corticosteroids regulate the gene expression of FGF-1 and FGF-2 in cultured rat astrocytes

The present data show that the gene expression of FGF-1 and FGF-2 is regula ted by corticosteroids in rat type 1 astrocytes. In particular, the gene ex pression of FGF-1 is modulated by corticosteroids acting both on type I (mi nerocorticoid) and type II (glucocorticoid) receptors. In fact, at short ti mes of exposure (2 h) a slight decrease in FGF-1 mRNA levels is induced by deoxycorticosterone, a steroid able to interact with the type I receptors; a similar effect is observed at 6 h following exposure to corticosterone or its 5 alpha -reduced metabolite, dihydrocorticosterone. Conversely, at lon ger times of exposure (24 h) corticosterone is able to strongly increase FG F-1 mRNA levels. Both effects of corticosterone (inhibition and stimulation ) were duplicated by dexamethasone, indicating that both effects occur via the type II receptors. Interestingly, the 5 alpha -3 alpha -reduced metabol ite of deoxycorticosterone, tetrahydrodeoxycorticosterone, which does not i nteract with either corticosteroid receptors, is able to stimulate (at 6 an d 24 h of exposure) the gene expression of FGF-1. It is possible that this effect might be induced via the GABA(A) receptor, since muscimol, an agonis t of this receptor, exerts a similar effect. The situation is different in the case of FGF-2. The mRNA levels of this gr owth factor are only stimulated by steroids interacting with type II recept ors. Altogether, these observations indicate that corticosteroids modulate the levels of FGF-1 and FGF-2 gene expression in astroglial cells by intera ction with classical (type I and II) or nonclassical (GABA(A) receptor) ste roid receptors.