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Search for other papers by O. M. Onagbesan in
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The effects of insulin-like growth factor I (IGF-I), alone, and in combination with LH or transforming growth factor α (TGF-α), on replication and progesterone production by cultured avian granulosa cells obtained from the three largest (F1–F3) follicles were studied. IGF-I and TGF-α stimulated proliferation of granulosa cells in a dose-dependent manner, and responsiveness decreased as the cells matured. IGF-I stimulated progesterone production from granulosa cells of all the follicles with no change in ED50 value during follicular maturation; however, the maximum response was from cells derived from F1 follicles. IGF-I plus LH had an additive effect on progesterone production by cells from all follicles. In contrast, TGF-α inhibited basal and LH- and IGF-I-stimulated progesterone production. These data show that IGF-I and TGF-α may interact with each other during granulosa cell maturation, such that efficacy of IGF-I increases, while that of TGF-α decreases before ovulation. Furthermore, both growth factors interact with LH, either to enhance or inhibit progesterone production by granulosa cells. However, LH, IGF-I and TGF-α combine to stimulate proliferation of granulosa cells.
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Summary. Suspensions of luteal cells were prepared by collagenase dispersion of guinea-pig corpora lutea obtained at specific times during the oestrous cycle. Luteal cells incubated with hCG produced increased amounts of progesterone. For Days 3–13 of the oestrous cycle, the concentrations of hCG required for 50% of the maximum response were within the range, 1 × 10−3 to 7 × 10−3 i.u./ml, showing no marked loss of sensitivity to hCG with increasing luteal age. PGF-2α (1 μmol/1), had no effect on basal production of progesterone but significantly inhibited hCG-stimulated progesterone production by luteal cells isolated on Days 7, 9, 10, 12 and 13 of the cycle. This concentration of PGF-2α had no significant effect on progesterone production by luteal cells prepared earlier in the cycle (Days 3 and 5). It is concluded that (a) the luteolytic action of PGF-2α in the guinea-pig is mediated, at least in part, by direct action on luteal cells, and (b) the cells from newly formed corpora luteal are resistant to the direct inhibitory action of PGF-2α.
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The purpose of this study was to determine the presence of epidermal growth factor receptor and its potential ligands epidermal growth factor (EGF) and transforming growth factor α (TGF-α) in the tissues of the maturing follicles in the ovary of laying ISA-Brown hens using peptide-specific immunohistochemical methods. Cryostat sections, 6–8 μm thick, were made from fresh–frozen tissues of F1–F4 (largest to fourth largest) and large white follicles and they were immunostained for epidermal growth factor receptor, epidermal growth factor or transforming growth factor α using specific polyclonal antibodies. The EGF receptor and both ligands were detected in the granulosa, theca interna and theca externa layers of the follicles. The EGF receptor was localized both in the plasma membrane and cytoplasm of all cell types. EGF was predominantly cytosolic, whereas TGF-α was found in the plasma membranes and perinuclear areas of all cell types. The concentration of the receptor and both ligands decreased with follicular maturation. This observation is consistent with our previous observation that the response to EGF and TGF-α decreases as follicles mature, and thus provides further evidence that the receptor or the ligands may have a regulatory role in avian ovarian function.
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Summary. Immature rats were treated with PMSG followed 56 h later by 10 i.u. hCG. Follicles were removed at intervals after hCG injection. Transient increases in progesterone, testosterone and oestradiol synthesis were first evident 1 h after hCG, but values peaked at 3–5 h and returned to control levels by 10 h. Increased synthesis of PGE-2 and PGF-2α was not evident until 3 h and peaked at more than 10 h after hCG. Ovulation began between 8 and 10 h after hCG and 83% of animals had ovulated within 12 h.
Doses of 90 or 1800 μg indomethacin given together with hCG substantially inhibited ovulation and PG synthesis, but only the higher dose inhibited the hCG-induced elevation of progesterone and testosterone synthesis; hCG-induced oestradiol synthesis was not affected by either dose of indomethacin.
We conclude that the peak of PG synthesis after hCG treatment related closely to the timing of ovulation; the steroidogenic response to hCG was not blocked by doses of indomethacin sufficient to inhibit synthesis of PGE-2 and PGF-2α by more than 80%.