Access

You are not currently logged in.

Access your personal account or get JSTOR access through your library or other institution:

login

Log in to your personal account or through your institution.

If You Use a Screen Reader

This content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.

Regulation of β -adrenergic Receptors by ``Permissive'' Hormones: Glucocorticoids Increase Steady-State Levels of Receptor mRNA

John R. Hadcock and Craig C. Malbon
Proceedings of the National Academy of Sciences of the United States of America
Vol. 85, No. 22 (Nov. 15, 1988), pp. 8415-8419
Stable URL: http://www.jstor.org/stable/32751
Page Count: 5
  • Read Online (Free)
  • Subscribe ($19.50)
  • Cite this Item
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Regulation of β -adrenergic Receptors by ``Permissive'' Hormones: Glucocorticoids Increase Steady-State Levels of Receptor mRNA
Preview not available

Abstract

Incubation of DDT1 MF-2 hamster vas deferens cells with glucocorticoids results in a marked increase in β -adrenergic receptor (β AR) number. The increase in receptor number was visualized by indirect immunofluorescence with antiserum specific for the β AR and was verified by radioligand binding. The steady-state levels of β AR mRNA were quantified in untreated (control) and glucocorticoid-treated cells by DNA-excess solution hybridization using a single-stranded probe corresponding to nucleotides +12 to 182 of the hamster β 2AR cDNA coding region. The steady-state level increased from 0.37 pg of β AR mRNA per μ g of total cellular RNA in untreated cells to 1.05 pg of β AR mRNA per μ g of RNA in cells treated with dexamethasone (500 nM) for 2-4 hr. After this sharp transient peak, the steady-state level of receptor mRNA declined by 6 hr to a level approximately twice that of the untreated cells. Half-maximal effects were achieved at 20-40 nM dexamethasone. Testosterone (500 nM) and 17β -estradiol (500 nM), in contrast, did not alter the steady-state levels of β AR mRNA. Actinomycin D, a potent inhibitor of transcription, abolished the dexamethasone-induced increase in β AR mRNA, suggesting that the permissive hormone effect was exerted on gene transcription. The half-life of the receptor mRNA measured in the presence of actinomycin D was found to be 12 hr in both the untreated and the dexamethasone-treated cells. These studies provide a molecular explanation for the well-known regulation of GTP-binding protein (G-protein)-linked cell-surface receptors by permissive hormones.

Page Thumbnails

  • Thumbnail: Page 
8415
    8415
  • Thumbnail: Page 
8416
    8416
  • Thumbnail: Page 
8417
    8417
  • Thumbnail: Page 
8418
    8418
  • Thumbnail: Page 
8419
    8419