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Regulation of β 2 ‐adrenergic receptors in keratinocytes: glucocorticoids increase steady‐state levels of receptor mRNA in foetal rat keratinizing epidermal cells (FRSK cells)
Author(s) -
TAKAHASHI H.,
IIZUKA H.
Publication year - 1991
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.1991.tb00594.x
Subject(s) - endocrinology , medicine , cyclase , adenylate kinase , cholera toxin , forskolin , receptor , biology , adrenergic receptor , chemistry , stimulation
Summary Glucocorticoids increase the β‐adrenergic adenylate cyclase response of epidermal keratinocytes. Using FRSK cells, a cultured cell line of foetal rat keratinocytes, the regulatory mechanism of the β‐adrenergic augmentation effect was investigated. Treatment with dexamethasone (1 × 10 −6 M)increased by 1.5‐fold the β‐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 β 2 ‐adrenergic receptor mRNA increased within 3 h. while actin‐, Gs‐α, Gi‐2α, Gi‐3α mRNA levels were unchanged. Testosterone. 17β‐oestradiol. and progesterone had no effect on either the β 2 ‐adrenergic adenylate cyclase response or the expression of β 2 ‐adrenergic receptor mRNA. The increase in the numbers of the β‐adrenergic receptors was visualized by immunofluorescence with an antibody specific for the β 2 ‐adrenergic receptor. Our results indicate that glucocorticoids regulate the β 2 ‐adrenergic adenylate cyclase response of FRSK cells through the enhanced expression of the receptor.