We have used rat cortical astrocytes in culture to investigate the signaling pathways involved in the regulation of fibroblast growth factor-2 (FGF-2) and one of its high affinity receptor FGF receptor-1 (FGFR-1). These cells represent a source of different neurotrophic factors and play important roles in physiological and pathological conditions of the central nervous system. FGF-2 mRNA levels are increased by stimulation of beta-adrenergic receptors or exposure to glucocorticoid hormones and these effects are additive to each other. The regulation of FGFR-1, highly expressed in cultured astroglial cells, appears to be different. Isoproterenol produced an elevation of FGFR-1 mRNA levels, whereas dexamethasone decreased its expression alone or in the presence of isoproterenol, suggesting that the glucocorticoid pathway may predominate over the cAMP-induced up-regulation of the receptor. FGF-2 over-expression may produce different cellular responses depending on the concomitant regulation of its receptor and the cell phenotype where these changes do occur. These mechanisms can contribute to adaptive changes taking place in the CNS in different physiological and pathological situations.

Differential regulation of FGF-2 and FGFR-1 in rat cortical astrocytes by dexamethasone and isoproterenol / M.A. Riva, R. Molteni, G. Racagni. - In: MOLECULAR BRAIN RESEARCH. - ISSN 0169-328X. - 57:1(1998 Jun 01), pp. 38-45.

Differential regulation of FGF-2 and FGFR-1 in rat cortical astrocytes by dexamethasone and isoproterenol

M.A. Riva
Primo
;
R. Molteni
Secondo
;
G. Racagni
Ultimo
1998

Abstract

We have used rat cortical astrocytes in culture to investigate the signaling pathways involved in the regulation of fibroblast growth factor-2 (FGF-2) and one of its high affinity receptor FGF receptor-1 (FGFR-1). These cells represent a source of different neurotrophic factors and play important roles in physiological and pathological conditions of the central nervous system. FGF-2 mRNA levels are increased by stimulation of beta-adrenergic receptors or exposure to glucocorticoid hormones and these effects are additive to each other. The regulation of FGFR-1, highly expressed in cultured astroglial cells, appears to be different. Isoproterenol produced an elevation of FGFR-1 mRNA levels, whereas dexamethasone decreased its expression alone or in the presence of isoproterenol, suggesting that the glucocorticoid pathway may predominate over the cAMP-induced up-regulation of the receptor. FGF-2 over-expression may produce different cellular responses depending on the concomitant regulation of its receptor and the cell phenotype where these changes do occur. These mechanisms can contribute to adaptive changes taking place in the CNS in different physiological and pathological situations.
Fibroblast growth factor; Gene expression; Glia; Glucocorticoid; Neuroprotection; Noradrenergic system
Settore BIO/14 - Farmacologia
1-giu-1998
Article (author)
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/184247
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