Abstract:These results indicate a synergistic effect of IGF-I and GH on differentiation and replication of human granulosa cells, and thus support a role of both GH and IGF-I in regulation of ovarian function.
“…This possibility is indicated by the greater proportion of bovine oocytes manifesting the markers of cytoplasmic maturation (for instance, the ability to decondense sperm chromatin and form sperm asters (Hyttel et al 1989)) in GH-treated cell populations (Izadyar et al 1997(Izadyar et al , 1998. Nuclear maturation is similarly enhanced by GH, since GH-treated bovine oocytes complete meiosis I faster and undergo zygote cleavage and blastocyst formation more frequently than untreated oocytes (Van der Westerlaken et al 1994, Izadyar et al 1996, 1998. This effect of GH is dependent upon cAMP and the presence of cumulus cells but is IGF-Iindependent (Bevers et al 1989, Zuelke & Brackett 1993, Izadyar et al 1997, 1998, Kolle et al 1998.…”
Section: Figurementioning
confidence: 93%
“…Nuclear maturation is similarly enhanced by GH, since GH-treated bovine oocytes complete meiosis I faster and undergo zygote cleavage and blastocyst formation more frequently than untreated oocytes (Van der Westerlaken et al 1994, Izadyar et al 1996, 1998. This effect of GH is dependent upon cAMP and the presence of cumulus cells but is IGF-Iindependent (Bevers et al 1989, Zuelke & Brackett 1993, Izadyar et al 1997, 1998, Kolle et al 1998. GHR mRNA and protein are, moreover, not detected in oocytes from secondary or tertiary follicles of the bovine ovary (Kolle et al 1998); thus, direct actions at the oocyte itself appear unlikely.…”
Section: Figurementioning
confidence: 93%
“…The paucity of IGF-I in human follicles (Mason et al 1990, Ovesen et al 1994, even those treated with GH, would suggest that IGF-I does not mediate steroidogenic effects of GH in humans. Indeed, IGF-I independence is also indicated by the synergistic effect of GH and IGF-I/ IGF-II on oestradiol production in human (Ovesen 1998) granulosa cells. However, IGF-I antibodies significantly inhibit GH effects on oestradiol production in human granulosa cells (Barreca et al 1993).…”
Section: Steroidogenesismentioning
confidence: 99%
“…The folliculogenic effect of GH, at least in human luteinized granulosa cells, is dependent upon FSH and independent of IGF-I (Ovesen et al 1994, Ovesen 1998). …”
GH, as its name suggests, is obligatory for growth and development. It is, however, also involved in the processes of sexual differentiation and pubertal maturation and it participates in gonadal steroidogenesis, gametogenesis and ovulation. It also has additional roles in pregnancy and lactation. These actions may reflect direct endocrine actions of pituitary GH or be mediated by its induction of hepatic or local IGF-I production. However, as GH is also produced in gonadal, placental and mammary tissues, it may act in paracrine or autocrine ways to regulate local processes that are strategically regulated by pituitary GH. The concept that GH is an important modulator of female reproduction is the focus of this review.
“…This possibility is indicated by the greater proportion of bovine oocytes manifesting the markers of cytoplasmic maturation (for instance, the ability to decondense sperm chromatin and form sperm asters (Hyttel et al 1989)) in GH-treated cell populations (Izadyar et al 1997(Izadyar et al , 1998. Nuclear maturation is similarly enhanced by GH, since GH-treated bovine oocytes complete meiosis I faster and undergo zygote cleavage and blastocyst formation more frequently than untreated oocytes (Van der Westerlaken et al 1994, Izadyar et al 1996, 1998. This effect of GH is dependent upon cAMP and the presence of cumulus cells but is IGF-Iindependent (Bevers et al 1989, Zuelke & Brackett 1993, Izadyar et al 1997, 1998, Kolle et al 1998.…”
Section: Figurementioning
confidence: 93%
“…Nuclear maturation is similarly enhanced by GH, since GH-treated bovine oocytes complete meiosis I faster and undergo zygote cleavage and blastocyst formation more frequently than untreated oocytes (Van der Westerlaken et al 1994, Izadyar et al 1996, 1998. This effect of GH is dependent upon cAMP and the presence of cumulus cells but is IGF-Iindependent (Bevers et al 1989, Zuelke & Brackett 1993, Izadyar et al 1997, 1998, Kolle et al 1998. GHR mRNA and protein are, moreover, not detected in oocytes from secondary or tertiary follicles of the bovine ovary (Kolle et al 1998); thus, direct actions at the oocyte itself appear unlikely.…”
Section: Figurementioning
confidence: 93%
“…The paucity of IGF-I in human follicles (Mason et al 1990, Ovesen et al 1994, even those treated with GH, would suggest that IGF-I does not mediate steroidogenic effects of GH in humans. Indeed, IGF-I independence is also indicated by the synergistic effect of GH and IGF-I/ IGF-II on oestradiol production in human (Ovesen 1998) granulosa cells. However, IGF-I antibodies significantly inhibit GH effects on oestradiol production in human granulosa cells (Barreca et al 1993).…”
Section: Steroidogenesismentioning
confidence: 99%
“…The folliculogenic effect of GH, at least in human luteinized granulosa cells, is dependent upon FSH and independent of IGF-I (Ovesen et al 1994, Ovesen 1998). …”
GH, as its name suggests, is obligatory for growth and development. It is, however, also involved in the processes of sexual differentiation and pubertal maturation and it participates in gonadal steroidogenesis, gametogenesis and ovulation. It also has additional roles in pregnancy and lactation. These actions may reflect direct endocrine actions of pituitary GH or be mediated by its induction of hepatic or local IGF-I production. However, as GH is also produced in gonadal, placental and mammary tissues, it may act in paracrine or autocrine ways to regulate local processes that are strategically regulated by pituitary GH. The concept that GH is an important modulator of female reproduction is the focus of this review.
“…Most in vivo effects of GH are accompa-nied by an increase in insulin-like growth factor I (IGF-I) concentrations in the blood [7][8][9][10] and follicular fluid [7,9]. In vitro, GH is able to amplify gonadotrophin action, stimulate follicular growth and steroidogenesis, and promote the replication of granulosa cells [11][12][13]. It also stimulates IGF-I release from cultured granulosa cells and follicles in a range of species [14][15][16][17] and from the perfused rabbit ovary [11].…”
The role of cAMP/protein kinase A (PKA)- and tyrosine kinase (TK)-dependent intracellular mechanisms in mediating the action of porcine growth hormone (GH) on insulin-like growth factor I (IGF-I) secretion by porcine ovarian granulosa cells was studied. It was observed that GH-induced stimulation of IGF-I secretion was accompanied by an increase in cAMP production. The stimulation of PKA by the addition of either a cAMP agonist or a phosphodiesterase inhibitor to the medium increased IGF-I release by the cells, indicating a direct stimulation of IGF-I release by cyclic nucleotides. Moreover, the stimulatory effect of GH on IGF-I was completely suppressed by the addition of the PKA blocker Rp-cAMPS. Neither TK blocker altered the basal IGF-I level, but both strongly suppressed the GH-induced increase in IGF-I accumulation. Taken together, these findings suggest that cAMP/PKA- and/or TK-dependent pathways may be involved in the mediation of GH action on IGF-I release by porcine granulosa cells.
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