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Abstract
The presence of epidermal growth factor receptors (EGF-R) and the ligands epidermal growth factor/transforming growth factor-α (EGF/TGFα) have been reported in mammalian ovaries where they are implicated in folliculogenesis and steroidogenesis. Evidence is presented to show that authentic EGF/TGFα receptors are expressed by the avian granulosa cells. The TGFα receptors (TGFα-R) from chicken granulosa cells were characterized by specific binding of 125I-human TGFα. In this study, competition with human EGF, human TGFα, human IGF-I, human basic fibroblast growth factor (bFGF) and insulin for 125I-human TGFα binding demonstrated that the avian granulosa cell TGFα-R binds human EGF with 300-fold lower affinity than human TGFα. IGF-I, bFGF and insulin did not displace bound 125I-TGFα. Scatchard analysis showed that a single class of high-affinity binding sites is present on the granulosa cells (K d 0·23 ± 0·009 nm). However, the number of binding sites altered during follicular maturation with a significant decline in the most mature follicle. These results go some way to explaining the basis for the changing sensitivity of avian granulosa cells to EGF/TGFα stimulation as they mature. In addition, the gonadotrophins, LH and FSH, increased the number of receptors in cultured granulosa cells and may therefore partially influence folliculogenesis and steroidogenesis through this route.
Journal of Endocrinology (1996) 149, 171–179
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Ethane dimethanesulphonate (EDS) is cytotoxic to Leydig cells in the adult rat. To investigate the role and regulation of apoptosis in the Leydig cell, EDS (100 mg/kg i.p.) was administered to adult male rats and the testes examined 6, 12, 18, 24, 48 and 72 h later. Numbers of Leydig cells, identified by 3 beta-hydroxysteroid dehydrogenase immuno-histochemistry started to fall by 12 h after EDS injection and were almost undetectable by 72 h. Apoptotic cells in the interstitium, visualised by in situ end labelling of DNA, increased in number to reach a maximum 24 h after injection of EDS, and were undetectable by 72 h. In many tissues the apoptosis-related gene products act in cohort: Bcl-2 and Bcl-xl promoting survival of a cell, whilst Bax promotes cell death often positively regulated by the tumour-suppressor gene p53. Western blot analysis showed that: (1) Bcl-2 and p53 were absent from interstitial Leydig cells but were expressed in the seminiferous tubules. (2) Bax protein although expressed in the interstitium was not present in the Leydig cells. (3) Bcl-xl in Leydig cells was transiently increased after EDS. In conclusion, EDS kills Leydig cells by apoptosis; however the control of Leydig cell death does not involve p53 or the Bcl-2 family members but may require other gene products yet to be identified.