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Estrogen Regulation of an Eosinophil Chemotactic Factor in the Immature Rat Uterus^*

YON H. LEE, ROBERT S. HOWE, SHING-JIA SHA, CORY TEUSCHER, DANIEL M. SHEEHAN and C. RICHARD LYTTLE

Department of Obstetrics and Gynecology, University of Pennsylvania School of Medicine, Philadelphia Pennsylvania 19104
National Center for Toxicological Research Jefferson, Arkansas 72079

Address requests for reprints to: Dr. C. Richard Lyttle, University of Pennsylvania, Department of Obstetrics/Gynecology, Division of Reproductive Biology, Room 306, John Morgan Building, Philadelphia, Pennsylvania 19104–6080.

Abstract

Associated with the generalized uterine growth stimulated by estradiol in the rat are specific responses including messenger RNA (mRNA) synthesis, protein synthesis, and peroxidase activity. The increase in peroxidase activity, although sensitive to inhibitors of RNA and protein synthesis, results from an estradiol-stimulated influx of eosinophils into the uterus. We postulated the existence of an estradiol-regulated uterine chemotactic factor, testing this by an in vitro chemotactic assay with eosinophils isolated from mature rats. Treatment of immature rats with 1 µg estradiol for 24 h resulted in a significant increase in eosinophil chemotaxis compared to uterine extracts of vehicle-treated rats. This increase was seen as early as 3 h after estradiol administration and was maximal at 24 h. The magnitude of the chemotactic response was dependent on the dose of estradiol administered (1–100 µg). Estrone or estriol treatment resulted in chemotactic activity greater than control but less than estradiol. Direct addition of estradiol to extracts of control animals did not increase chemotaxis. The estradiolstimulated chemotaxis was blocked by in vivo treatment with the antiestrogen tamoxifen and by inhibitors of RNA and protein synthesis. Analysis of extracts from estradiol-treated uteri shows that the chemotactic factor is heat labile, pronase sensitive, and has a mass of approximately 20 kilodaltons (kDa). These data suggest that the estradiol-stimulated influx of eosinophils into the rat uterus is mediated by the synthesis, modification, or release of a protein whose synthesis is estradiol receptor mediated.

Footnotes

^* This work was supported by NIH Grants HD-20025 and HD-06274 (to C.R.L.), HD-21926 (to C.T.), and a grant from the Andrew F. Mellon Foundation.

Current address: Department of Obstetrics/Gynecology, Yonsei University, Seoul, South Korea.

Current address: Department of Obstetrics/Gynecology, Baystate Medical Center, Springfield, Massachusetts 01199.

Received July 13, 1989.

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