Previous reports have confirmed that steroid hormones modulate the expression of adrenergic receptors on the surface of smooth muscle myocytes. The present study was undertaken to evaluate the mechanism by which testosterone modulates alpha-1 adrenergic receptor expression in the DDT1 MF-2 transform
Glucocorticoid induction of β-adrenergic receptors in the DDT1MF-2 smooth muscle cell line involves synthesis of new receptor
✍ Scribed by James S. Norris; Pamela Brown; Jeffrey Cohen; Lawrence E. Cornett; Peter O. Kohler; Stewart L. MacLeod; Keith Popovich; Robert B. Robey; Mark Sifford; Allen J. Syms; Roy G. Smith
- Publisher
- Springer
- Year
- 1987
- Tongue
- English
- Weight
- 529 KB
- Volume
- 74
- Category
- Article
- ISSN
- 0300-8177
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✦ Synopsis
We have shown that glucocorticoids induce the appearance of beta 2-adrenergic receptors in membranes of the ductus deferens smooth muscle cell line (DDT1 MF-2). A concomitant increase in isoproterenol stimulated adenylate cyclase activity in the absence of exogenously applied GTP was observed as was a significantly increased (p less than 0.05) sensitivity of the adenylate cyclase system to exogenously applied GTP. However, no significant difference in the maximal velocity of adenylate cyclase between control and steroid treatment was measurable in the presence of sodium fluoride. Induction of beta 2-adrenergic receptors in DDT1 MF-2 cells is correlated with the presence of steroid receptors (androgen and glucocorticoid) in the cells since estrogens and progesterones had no effect on receptor levels. Finally, utilizing dense amino acid labeling of cells to measure old versus newly synthesized receptor sites by a density shift method, we have documented that glucocorticoid induction of beta 2-adrenergic receptors involves synthesis of new receptor protein.
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