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Endocrinology Vol. 139, No. 3 961-966
Copyright © 1998 by The Endocrine Society

ARTICLES

Mediators of Estradiol-Stimulated Mitosis in the Rat Uterine Luminal Epithelium1

Zhiming Zhang2, Jane Laping, Stanley Glasser, Peter Day and Joy Mulholland

Department of Cell Biology, Baylor College of Medicine (Z.Z., J.L., S.G., J.M.), Houston, Texas 77030; and the Department of Obstetrics and Gynecology, Thomas Jefferson University (P.D., J.M.), Philadelphia, Pennsylvania 19107

Address all correspondence and requests for reprints to: Dr. Joy Mulholland, Department of Obstetrics and Gynecology, Thomas Jefferson University, 834 Chestnut Street, Suite 400, Philadelphia, Pennsylvania 19107. E-mail: mulholl2{at}jeflin.tju.edu

The effects of estradiol treatment, which stimulates cell division in rat uterine epithelial cells, on the in vivo expression of heparin-binding epidermal growth factor (HB-EGF), cyclin D1, and cyclin B1 messenger RNA (mRNA) in these cells have been examined using ribonuclease protection assays. Estradiol gave rise to significant increases in steady state levels of HB-EGF 2 and 24 h after treatment. Cyclin D1 mRNA levels were elevated 8 and 10 h after estradiol administration, corresponding to the G1 phase of the mitotic cycle, and cyclin B1 mRNA was only expressed 16–24 h after estradiol treatment, which corresponds to the G2 and M phases of the rat uterine epithelial cell cycle. Estradiol-stimulated increases in HB-EGF mRNA were not affected by treatment with cycloheximide, but were inhibited by the estrogen antagonist compound, ICI 164,384, demonstrating that the estrogen-stimulated increase in HB-EGF mRNA is a primary, estrogen receptor-mediated response of rat uterine epithelium to estradiol. Progesterone treatment, which blocks epithelial cells in G1 of the cycle, suppressed levels of HB-EGF mRNA below those observed in ovariectomized rats. These results indicate that HB-EGF mediates the regulatory effects of both estradiol and progesterone on rat uterine epithelial cell proliferation through an effect on the production of G1 phase molecules such as cyclin D1.




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