| Autor: |
Buchanan, Clint D., Mahesh, Virendra B., Brann, Darrell W. |
| Zdroj: |
Biology of Reproduction; June 2000, Vol. 62 Issue: 6 p1710-1721, 12p |
| Abstrakt: |
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-β1(TGF-β1) and 3α-hydroxy-5α-pregnane-20-one (3α,5α-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-α 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-β antibody dose-dependently attenuated the LHRH-releasing activity of the CM. Rat hypothalamus and GT1–7 cells were demonstrated to express TGF-β receptors as well as furin, an enzyme that converts latent TGF-β1to active TGF-β1. Estrogen receptor-α and ER-β mRNA and protein were also demonstrated in HAs by reverse transcription-polymerase chain reaction and double immunofluorescence, and treatment with 17β-estradiol (17β-E2) increased both active and latent TGF-β1levels in HA CM. The effect of 17β-E2was completely blocked by the ER antagonist ICI8280. As a whole, these studies provide evidence of a previously undescribed 17β-E2-TGF-β1-LHRH signaling pathway. |
| Databáze: |
Supplemental Index |
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