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Department of Pharmacology The University of Texas Medical School at Houston Houston, Texas 77225
Address requests for reprints to: George M. Stancel, Department of Pharmacology, University of Texas Medical School, P.O. Box 20708, Houston, Texas 77225
Abstract
Previous studies have demonstrated that 17β-estradiol (E2) causes a 3-fold increase in epidermal growth factor (EGF) receptors in uterine membranes. We now report that the increase in uterine EGF receptor levels is due to an increase in the steady-state levels of EGF receptor mRNA. After a single E2 injection, EGF receptor mRNA levels, as determined by RNA blots, increase 3- to 4-fold between 1 and 3 h, remain elevated at 6 h, and decline between 12 and 18 h. The effect is specific for E2 since the nonestrogenic hormones progesterone, dexamethasone, 5
-dihydrotestosterone, and the inactive stereoisomer of E2, 17-estradiol, are without effect. E2-Mediated increases in EGF receptor mRNA levels are blocked by actinomycin D but not by puromycin. Taken together, these results indicate that E2 regulates the level of EGF receptor by increasing the steady-state concentration of EGF receptor mRNA in vivo.
FOOTNOTES
This work was supported by NIH Grants HD-08615, DK-38965, and RR-01685 (Bionet) for computer use.
Received for publication October 19, 1987. Accepted for publication November 30, 1987.
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