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Estrogen-Astrocyte-Luteinizing Hormone-Releasing Hormone Signaling: A Rolefor Transforming Growth Factor-ß₁¹

^a Department of Physiology & Endocrinology, School of Medicine, Medical College of Georgia, Augusta, Georgia 30912-3000

ABSTRACT

The purpose of this study was to identify factors from astrocytes that can regulate LHRH neurosecretion. Exposure of LHRH-secreting (GT1–7) cells to conditioned media (CM) from C6 glial cells and hypothalamic astrocytes (HA) stimulated LHRH release. Assays of C6 and HA CM revealed that transforming growth factor-ß₁ (TGF-ß₁) and 3-hydroxy-5-pregnane-20-one (3,5-THP), both known LHRH secretagogues, were present in CM and their levels increased in parallel to the LHRH-releasing activity of CM. In contrast, TGF- was undetectable in C6 or HA CM. Ultrafiltration to remove peptides with molecular weights >10 kDa virtually abolished the LHRH-releasing ability of the HA CM. Furthermore, immunoneutralization with a panspecific THF-ß antibody dose-dependently attenuated the LHRH-releasing activity of the CM. Rat hypothalamus and GT1–7 cells were demonstrated to express TGF-ß receptors as well as furin, an enzyme that converts latent TGF-ß₁ to active TGF-ß₁. Estrogen receptor- and ER-ß mRNA and protein were also demonstrated in HAs by reverse transcription-polymerase chain reaction and double immunofluorescence, and treatment with 17ß-estradiol (17ß-E₂) increased both active and latent TGF-ß₁ levels in HA CM. The effect of 17ß-E₂ was completely blocked by the ER antagonist ICI8280. As a whole, these studies provide evidence of a previously undescribed 17ß-E₂-TGF-ß₁-LHRH signaling pathway.

FOOTNOTES

First decision: 20 December 1999.

¹ This research was conducted as part of the requirements for completion of the Ph.D. degree and was supported by a research grant (HD-28964) from the NIH/NICHHD. C.B.'s research was also supported by an NRSA Institutional Training Grant (HD07253) from the NIH/NICHHD.

² Correspondence. FAX: 706 721 7299; dbrann{at}mail.mcg.edu

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