Stimulation of RNA synthesis in corpora lutea nuclei by human chorionic gonadotropin in vitro

1974 ◽  
Vol 349 (3) ◽  
pp. 465-468 ◽  
Author(s):  
Kenneth W. McKerns
Keyword(s):  
Chorionic Gonadotropin ◽  
Human Chorionic Gonadotropin ◽  
Rna Synthesis ◽  
Corpora Lutea ◽  
Stimulation Of

scholarly journals Connective Tissue Growth Factor Expression in the Human Corpus Luteum: Paracrine Regulation by Human Chorionic Gonadotropin

2005 ◽  
Vol 90 (9) ◽  
pp. 5366-5376 ◽  
Author(s):  
W. Colin Duncan ◽  
Stephen G. Hillier ◽  
Eva Gay ◽  
Julie Bell ◽  
Hamish M. Fraser
Keyword(s):  
Growth Factor ◽  
Connective Tissue ◽  
Chorionic Gonadotropin ◽  
Granulosa Cells ◽  
Human Chorionic Gonadotropin ◽  
Luteal Phase ◽  
Primary Cultures ◽  
Tissue Growth ◽  
Corpora Lutea

Abstract Context: The molecular mechanisms of luteolysis and its inhibition during maternal recognition of pregnancy remain unclear. Objective: The objective of this study was to investigate the differential regulation of connective tissue growth factor (CTGF) expression in human corpora lutea using in vivo and in vitro models. Design: Corpora lutea from different stages of the luteal phase and after luteal rescue with human chorionic gonadotropin (hCG) were studied. Primary cultures and cocultures of luteinized granulosa cells and luteal fibroblast-like cells were performed. Setting: This study was performed at the research center of a university teaching hospital. Patients: Women with regular cycles having hysterectomy for nonmalignant conditions and women undergoing oocyte collection for assisted conception were studied. Interventions: CTGF localization was determined by in situ hybridization, and expression by quantitative RT-PCR. Outcomes: The outcome measures were the effect of hCG on the expression and localization of CTGF mRNA in human corpora lutea and the effect of hCG on CTGF expression in primary cultures of luteinized granulosa cells and luteal fibroblast-like cells. Results: Luteal rescue reduced CTGF expression compared with that in the late luteal phase (P < 0.05). CTGF expression was localized to fibroblast-like cells and endothelial cells of larger blood vessels, not to steroidogenic cells. The expression of CTGF by fibroblast-like cells in vitro was not regulated by hCG. When cocultured with luteinized granulosa cells, fibroblast-like cell CTGF expression was inhibited by hCG (P < 0.001). This effect was independent of stimulated progesterone concentrations and was not blocked by follistatin or indomethacin. Both IL-1α (P < 0.05) and cAMP (P < 0.001) inhibited CTGF expression in fibroblast-like cells. Conclusions: These results provide evidence for negative regulation of CTGF by hCG during luteal rescue mediated by paracrine signals.

scholarly journals Priming with a gonadotropin-releasing hormone agonist before immature oocyte retrieval may improve maturity of oocytes and outcome in in vitro maturation (IVM) cycle: a case report

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
A. Smirnova ◽  
M. Anshina ◽  
E. Shalom Paz ◽  
A. Ellenbogen
Keyword(s):  
Fertility Preservation ◽  
Chorionic Gonadotropin ◽  
Human Chorionic Gonadotropin ◽  
Oocyte Retrieval ◽  
Fertilization Rate ◽  
Gonadotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Nuclear Maturation ◽  
Gonadotropin Releasing Hormone Agonist

Abstract Background The concept of using a gonadotropin-releasing hormone agonist (GnRH-a) instead of human chorionic gonadotropin for triggering ovulation in patients treated with an antagonist protocol for in vitro fertilization (IVF) has become a routine clinical practice. It may promote oocyte nuclear maturation, resumption of meiosis and cumulus expansion. It seems that this attempt could be beneficial in an in vitro maturation (IVM) oocyte cycle performed for polycystic ovarian syndrome as well as for other indications such as urgent fertility preservation in patients with malignancies or unusual indications. Case presentation We present the case of a Caucasian patient who needed fertility preservation when routine natural IVF treatment did not yield oocyte retrieval, followed by three IVM cycles, priming ovulation with a GnRH-a. In total, 12 oocytes were obtained, all matured 4.5 hours after incubation in maturation media. The fertilization rate after intracytoplasmic sperm injection was 83%. Six good-quality embryos were vitrified. Conclusions It seems that triggering with a GnRH-a in selected cases may replace human chorionic gonadotropin in IVM of oocytes and could be highly beneficial in terms of obtaining high-grade embryos and possible pregnancy.

scholarly journals Biosynthesis of growth hormone in the rat anterior pituitary gland. Stimulation of biosynthesis in vitro by insulin

1973 ◽  
Vol 134 (4) ◽  
pp. 1103-1113 ◽  
Author(s):  
A. Betteridge ◽  
M. Wallis
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Rna Synthesis ◽  
Glucose Utilization ◽  
Actinomycin D ◽  
Hormone Synthesis ◽  
Pituitary Glands ◽  
Hormone Biosynthesis ◽  
Stimulation Of

The effect of insulin on the incorporation of radioactive leucine into growth hormone was investigated by using rat anterior pituitary glands incubated in vitro. A 50% stimulation over control values was observed at insulin concentrations above 2μm (280munits/ml). The effect was specific for growth hormone biosynthesis, over the range 1–5μm-insulin (140–700munits/ml). Lower more physiological concentrations had no significant effect in this system. Above 10μm (1.4 units/ml) total protein synthesis was also increased. The stimulation of growth hormone synthesis could be partially blocked by the addition of actinomycin D, suggesting that RNA synthesis was involved. Insulin was found to stimulate the rate of glucose utilization in a similar way to growth hormone synthesis. 2-Deoxyglucose and phloridzin, which both prevented insulin from stimulating glucose utilization, also prevented the effect of insulin on growth hormone synthesis. If glucose was replaced by fructose in the medium, the effect of insulin on growth hormone synthesis was decreased. We conclude that the rate of utilization of glucose may be an important step in mediating the effect of insulin on growth hormone synthesis.

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