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Retinoid-induced beta-adrenergic inhibitory effect associated with increased thymidine incorporation of fetal rat keratinizing epidermal cells (FRSK cells).

Abstract：

:Using fetal rat keratinizing epidermal cells (FRSK cells) we investigated the effects of retinoids on the cyclic AMP system. The beta-adrenergic adenylate cyclase response was significantly decreased by the treatment of cells with 1 x 10(-6) M Ro 10-1670. The effect was observed by 12 h and remained for at least 48 h. The decreased beta-adrenergic response was accompanied by increased adenosine- and forskolin-induced cyclic AMP accumulations. Thymidine incorporation of FRSK cells was also increased by the retinoid treatment. Northern blot hybridization showed that none of the messages (the beta2-adrenergic receptor, the stimulatory guanine nucleotide binding protein (Gs-alpha), or the inhibitory guanine nucleotide binding proteins (Gi-2 alpha, Gi-3 alpha)) were significantly altered by the retinoid treatment. We have already reported that the beta-adrenergic response as well as the beta2-adrenergic receptor mRNA is increased by the dexamethasone treatment of FRSK cells. The addition of both Ro 10-1670 and dexamethasone in the incubation medium resulted in the loss of the beta-adrenergic augmentation effect by dexamethasone. These results indicate that retinoids decrease the beta-adrenergic response and increase the thymidine incorporation of FRSK cells. This is contrary to the previous results using pig epidermal organ culture system.

journal_name

J Dermatol Sci

journal_title

Journal of dermatological science

authors

Takahashi H,Iizuka H

doi

10.1016/0923-1811(93)90080-9

subject

Has Abstract

pub_date

1993-04-01 00:00:00

pages

122-9

issue

2

eissn

0923-1811

issn

1873-569X

pii

0923-1811(93)90080-9

journal_volume

5

pub_type

杂志文章

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