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Estrogens Increase the Number of Thyrotropin-Releasing Hormone Receptors on Mammotropic Cells in Culture^*

MARVIN C. GERSHENGORN, BERNICE E. MARCUS-SAMUELS and ELIZABETH GERAS

Endocrine Division, Department of Medicine, New York University Medical Center New York, New York 10016

Address requests for reprints to: Dr. M. C. Gershengorn, Bellevue C & D, Room 614, New York University Medical Center, 550 First Avenue, New York, New York 10016.

Abstract

The number of plasma membrane receptors for TRH on tumor-derived mammotropic cells in culture, GH.i and GC cells, but not their affinity for TRH, was increased by estrogens. For GH₃ cells, exposure to 10 nM 17β-estradiol for 48 h increased the receptor level from 54,000 to 90,000 sites/cell, while for GC cells, the number of receptors increased from 29,000 to 46,000 after 28 h. PRL accumulation in the medium was also increased by 17β-estradiol. 17β-Estradiol and diethylstilbestrol were equally potent in increasing the TRH receptor level, while estrone was only l/10th as potent. Diethylstilbestrol bound to the cytoplasmic estrogen receptor with an apparent affinity approximately 2.5 times higher than 17β-estradiol in GH₃ and GC cells, while the affinity for estrone was only 1/12th to 1/20th that of 17β/8-estradiol. Tamoxifen, an antiestrogenic compound, inhibited the increase in TRH receptor number induced by 0.3 nM 17β/8-estradiol and was capable of binding to the estrogen receptor. Modulation of the TRH receptor level on mammotropic cells by estrogens, which is likely mediated through cytoplasmic estrogen receptors, may be an important mechanism for regulation of TRH action

Footnotes

^* This work was supported by Grants Am-20249 and SO-7RR5399 from the USPHS.

Recipient of NIH Research Career Development Award AM- 00566.

Received September 12, 1978.

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