Regulation of β2-adrenergic receptors in keratinocytes: glucocorticoids increase steady-state levels of receptor mRNA in foetal rat keratinizing epidermal cells (FRSK cells)

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Abstract
Glucocorticoids increase the beta-adrenergic adenylate cyclase response of epidermal keratinocytes. Using FRSK cells, a cultured cell line of foetal rat keratinocytes, the regulatory mechanism of the beta-adrenergic augmentation effect was investigated. Treatment with dexamethasone (1 x 10(-6) M increase by 1.5-fold the beta-adrenergic adenylate cyclase response of FRSK cells. The effect was observed at 6 h incubation and remained for at least 48 h. The prostaglandin E-adenylate cyclase response was also increased 1.5-fold by glucocorticoid treatment. Neither the adenosine-adenylate cyclase response nor cholera toxin- or forskolin-induced cyclic AMP accumulations were altered. Northern blot hybridization showed that levels of the beta 2-adrenergic receptor mRNA increased within 3 h, while actin-, Gs-alpha, Gi-2 alpha, Gi-3 alpha mRNA levels were unchanged. Testosterone, 17 beta-oestradiol, and progesterone had no effect on either the beta 2-adrenergic adenylate cyclase response or the expression of beta 2-adrenergic receptor mRNA. The increase in the numbers of the beta-adrenergic receptors was visualized by immunofluorescence with an antibody specific for the beta 2-adrenergic receptor. Our results indicate that glucocorticoids regulate the beta 2-adrenergic adenylate cyclase response of FRSK cells through the enhanced expression of the receptor.

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