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Regulation of Dexras1 expression by endogenous steroids

M D Brogan1, E N Behrend, R J Kemppainen

  • 1Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, AL 36849, USA.

Neuroendocrinology
|October 13, 2001
PubMed

Insights

Dexras1 gene expression is induced by glucocorticoids in AtT-20 cells. However, in mouse pituitaries, both glucocorticoids and beta-estradiol (E2) stimulate Dexras1 expression, suggesting differential regulation.

Area of Science:

  • Molecular endocrinology
  • Gene expression regulation
  • Steroid hormone signaling

Background:

  • Dexras1, a novel Ras superfamily protein, is rapidly induced by glucocorticoids in AtT-20 corticotrope cells.
  • Its function remains unknown, but induction suggests a role in negative feedback of corticotropin secretion.

Purpose of the Study:

  • To investigate the regulatory mechanisms controlling Dexras1 gene expression.
  • To determine the effects of various steroid hormones on Dexras1 expression in AtT-20 cells and mouse pituitaries.

Main Methods:

  • Treatment of AtT-20 cells and mice with six different steroids: aldosterone, corticosterone, dexamethasone, beta-estradiol, progesterone, and testosterone.
  • Assessment of Dexras1 expression using reverse transcription polymerase chain reaction (RT-PCR) and Northern analysis.

Main Results:

  • In AtT-20 cells, only glucocorticoids (dexamethasone and corticosterone) induced Dexras1 expression.
  • In mouse pituitaries, both glucocorticoids and beta-estradiol (E2) significantly increased Dexras1 expression.
  • Other tested steroids had no effect on Dexras1 expression in either model.

Conclusions:

  • Dexras1 expression in AtT-20 corticotropes is primarily regulated by glucocorticoids.
  • Dexras1 expression in the mouse pituitary gland is also responsive to beta-estradiol (E2).
  • These findings suggest differential regulation of Dexras1 expression between AtT-20 cells and mouse pituitary, potentially involving cell-specific mechanisms or expression in non-corticotrope pituitary cells.

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