1988
DOI: 10.1016/s0167-7306(08)60664-x
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Chapter 9 Mechanism of action of FSH in the ovary

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Cited by 3 publications
(5 citation statements)
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“…In mammals, FSH stimulates aromatase activity in the granulosa cells, thereby enhancing E production [59][60]. In salmon, as in mammals, cells in the thecal layer produce testosterone (T), which is converted to E by aromatase in granulosa layers during vitellogenesis [45,50,[56][57][58].…”
Section: Ovarymentioning
confidence: 99%
“…In mammals, FSH stimulates aromatase activity in the granulosa cells, thereby enhancing E production [59][60]. In salmon, as in mammals, cells in the thecal layer produce testosterone (T), which is converted to E by aromatase in granulosa layers during vitellogenesis [45,50,[56][57][58].…”
Section: Ovarymentioning
confidence: 99%
“…Studies of the intracellular mechanisms by which FSH and LH regulate granulosa cell function have focused primarily upon the activation of adenylate cyclase with subsequent increases in cAMP and CAMPdependent protein kinase activity (Hsueh et al, 1985;Dahl and Hsueh, 1988;Amsterdam et al, 1989). How- ever, recent investigations have raised the possibility of alternate intracellular mechanisms, since stimulation with gonadotropins has been shown to stimulate PtdIns turnover (Davis et al, 1983(Davis et al, , 1984 and calcium influx in granulosa cells (Veldhuis and Klase, 1982;Veldhuis et al, 1984;Asem et al, 1987;Alila et al, 1989;Flares et al, 1990).…”
Section: Discussionmentioning
confidence: 99%
“…Since increased GPI labelling is accompanied by concomitant increases in hCG binding (Fig. 6), it is tempting to speculate that the observed augmentation in GPI content elicited by FSH might be another of the hormone associated events related with granulosa cell differentiation and LH/hCG receptor induction (Hsueh et al, 1985; Dahl and Hsueh, 1988). This hypothesis seems reasonable since ( 1) similar increases in glycosyl-phosphatidylinositol content have been reported after PHA induced increase in insulin receptor number in lymphocytes (Gaulton et al, 1988) or in stably transfected CHO cells overexpressing the human insulin receptor (Villalba et al, 1990); (2) treatment of cells with the protein kinase C-activating phorbol ester, an agent known to prevent granulosa cell differentiation (Welsh et al, 1984b;Shinohara et al, 1985); Ben-Ze'ev and ) is accompanied by a time-related decrease in GPI labelling (Fig.…”
Section: Discussionmentioning
confidence: 99%
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