Estradiol and Gonadotropin-Releasing Hormone (GnRH) Interact to Increase GnRH Receptor Expression in Ovariectomized Ewes After Hypothalamic-Pituitary Disconnection

Endocrine ◽  
1998 ◽  
Vol 8 (3) ◽  
pp. 225-230 ◽  
Author(s):  
Bridgette L. Kirkpatrick ◽  
Eduardo Esquivel ◽  
Gary E. Moss ◽  
Debora L. Hamernik ◽  
Mark E. Wise
Keyword(s):  
Gnrh Receptor ◽  
Gonadotropin Releasing Hormone ◽  
Receptor Expression ◽  
Releasing Hormone

scholarly journals Gonadotropin-releasing hormone and its receptor in normal and malignant cells

2004 ◽  
Vol 11 (4) ◽  
pp. 725-748 ◽  
Author(s):  
G S Harrison ◽  
M E Wierman ◽  
T M Nett ◽  
L M Glode
Keyword(s):  
Cancer Cells ◽  
Hypogonadotropic Hypogonadism ◽  
Current Data ◽  
Gnrh Receptor ◽  
Gonadotropin Releasing Hormone ◽  
Receptor Expression ◽  
Sex Steroid ◽  
Endocrine Disorders ◽  
Sex Steroid Hormone ◽  
Releasing Hormone

Gonadotropin-releasing hormone (GnRH) is the hypothalamic factor that mediates reproductive competence. Intermittent GnRH secretion from the hypothalamus acts upon its receptor in the anterior pituitary to regulate the production and release of the gonadotropins, LH and FSH. LH and FSH then stimulate sex steroid hormone synthesis and gametogenesis in the gonads to ensure reproductive competence. The pituitary requires pulsatile stimulation by GnRH to synthesize and release the gonadotropins LH and FSH. Clinically, native GnRH is used in a pump delivery system to create an episodic delivery pattern to restore hormonal defects in patients with hypogonadotropic hypogonadism. Agonists of GnRH are delivered in a continuous mode to turn off reproductive function by inhibiting gonadotropin production, thus lowering sex steroid production, resulting in medical castration. They have been used in endocrine disorders such as precocious puberty, endometriosis and leiomyomata, but are also studied extensively in hormone-dependent malignancies. The detection of GnRH and its receptor in other tissues, including the breast, ovary, endometrium, placenta and prostate suggested that GnRH agonists and antagonists may also have direct actions at peripheral targets. This paper reviews the current data concerning differential control of GnRH and GnRH receptor expression and signaling in the hypothalamic–pituitary axis and extrapituitary tissues. Using these data as a backdrop, we then review the literature about the action of GnRH in cancer cells, the utility of GnRH analogs in various malignancies and then update the research in novel therapies targeted to the GnRH receptor in cancer cells to promote anti-proliferative effects and control of tumor burden.

The effect of inflammation on the synthesis of luteinizing hormone and gonadotropin-releasing hormone receptor expression in the pars tuberalis of ewe during different photoperiodic conditions

2018 ◽  
Vol 98 (4) ◽  
pp. 675-687 ◽  
Author(s):  
Karolina Wojtulewicz ◽  
Dorota Tomaszewska-Zaremba ◽  
Agata Krawczyńska ◽  
Monika Tomczyk ◽  
Andrzej Przemysław Herman
Keyword(s):  
Gene Expression ◽  
Luteinizing Hormone ◽  
Follicular Phase ◽  
Gnrh Receptor ◽  
Gonadotropin Releasing Hormone ◽  
Receptor Expression ◽  
Pars Tuberalis ◽  
Type I ◽  
Releasing Hormone ◽  
Gene And Protein Expression

The study was designed to determine the effect of endotoxin-induced inflammation on luteinizing hormone (LH) synthesis and gonadotropin-releasing hormone (GnRH) receptor expression in the pars tuberalis (PT) of ewes during anestrous season and follicular phase taking into account the time of the day. Moreover, the effect of inflammation on the release of melatonin and its type I receptor gene expression in the PT was also determined. Lipopolysaccharide administration reduced nocturnal release of melatonin only during anestrous season, but it did not influence the gene expression of melatonin type I receptor in the PT. Inflammation inhibited nocturnal increase in the gene and protein expression of LH in the PT during the follicular phase. Since in day-active species nocturnal accumulation of LH protein in the pituitary precedes the LH surge, this lowering of LH content may delay or disturb the surge occurrence. Suppression of LH secretion could have resulted from the decreased sensitivity of the PT on the action of GnRH because inflammation reduced GnRH receptor expression. The study suggests that the ability of endotoxin to suppress LH synthesis in the PT may be another mechanism by which inflammation disturbs reproductive neuroendocrine axis in seasonal breeders.

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