β2-Adrenergic receptors in hamster smooth muscle cells are transcriptionally regulated by glucocorticoids

Published

Journal Article

Steroid hormones modulate adrenergic receptor responsiveness and receptor number. To investigate the regulation of the β2-adrenergic receptor gene by glucocorticoids we examined the effects of the synthetic glucocorticoid agonist triamcinolone acetonide on the expression of β2-adrenergic receptors in DDT1MF-2 hamster smooth muscle cells. Glucocorticoid treatment (1 x 10-7 M) produced a 2.2 ± 0.4-fold (n = 8) increase in β2-adrenergic receptor number (maximum between 6 and 12 h) as determined by radioligand binding and a similar increase in catecholamine-stimulated adenylate cyclase activity. Steady-state levels of β2-adrenergic receptor mRNA, analyzed by Northern blot hybridization, were increased 2.4 ± 0.4-fold (n = 6) within 1 h, while actin mRNA levels were unchanged throughout the experiment. These steroid-induced increases in β2-adrenergic receptor mRNA returned to control levels by 24 h and were followed by a much slower decline in β2-adrenergic receptor in plasma membranes. The rate of β2-adrenergic receptor gene transcription, assessed by nuclear run-off transcription assays, increased 3.1 ± 0.1-fold (n = 2) in cells treated for 30 min with 1 x 10-7 M triamcinolone acetonide. These studies indicate that glucocorticoids regulate the β2-adrenergic receptor-adenylate cyclase system by controlling the rate of transcription of the β2-adrenergic receptor gene and hence the responsiveness of the enzyme to catecholamine stimulation.

Duke Authors

Cited Authors

  • Collins, S; Caron, MG; Lefkowitz, RJ

Published Date

  • January 1, 1988

Published In

Volume / Issue

  • 263 / 19

Start / End Page

  • 9067 - 9070

International Standard Serial Number (ISSN)

  • 0021-9258

Citation Source

  • Scopus