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.

Effects of corticotropin-releasing hormone and its antagonist on the gene expression of gonadotrophin-releasing hormone (GnRH) and GnRH receptor in the hypothalamus and anterior pituitary gland of follicular phase ewes

2011 ◽  
Vol 23 (6) ◽  
pp. 780 ◽  
Author(s):  
Magdalena Ciechanowska ◽  
Magdalena Łapot ◽  
Tadeusz Malewski ◽  
Krystyna Mateusiak ◽  
Tomasz Misztal ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Follicular Phase ◽  
Gnrh Receptor ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion ◽  
Crh Receptors

There is no information in the literature regarding the effect of corticotropin-releasing hormone (CRH) on genes encoding gonadotrophin-releasing hormone (GnRH) and the GnRH receptor (GnRHR) in the hypothalamus or on GnRHR gene expression in the pituitary gland in vivo. Thus, the aim of the present study was to investigate, in follicular phase ewes, the effects of prolonged, intermittent infusion of small doses of CRH or its antagonist (α-helical CRH 9-41; CRH-A) into the third cerebral ventricle on GnRH mRNA and GnRHR mRNA levels in the hypothalamo–pituitary unit and on LH secretion. Stimulation or inhibition of CRH receptors significantly decreased or increased GnRH gene expression in the hypothalamus, respectively, and led to different responses in GnRHR gene expression in discrete hypothalamic areas. For example, CRH increased GnRHR gene expression in the preoptic area, but decreased it in the hypothalamus/stalk median eminence and in the anterior pituitary gland. In addition, CRH decreased LH secretion. Blockade of CRH receptors had the opposite effect on GnRHR gene expression. The results suggest that activation of CRH receptors in the hypothalamus of follicular phase ewes can modulate the biosynthesis and release of GnRH through complex changes in the expression of GnRH and GnRHR genes in the hypothalamo–anterior pituitary unit.

scholarly journals Melatonin inhibits hypothalamic gonadotropin-releasing hormone release and reduces biliary hyperplasia and fibrosis in cholestatic rats

2017 ◽  
Vol 313 (5) ◽  
pp. G410-G418 ◽  
Author(s):  
Matthew McMillin ◽  
Sharon DeMorrow ◽  
Shannon Glaser ◽  
Julie Venter ◽  
Konstantina Kyritsi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Liver Injury ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Serum Levels ◽  
Gnrh Receptor ◽  
Gonadotropin Releasing Hormone ◽  
Cholestatic Liver Disease ◽  
Releasing Hormone ◽  
The Brain

Melatonin is a hormone produced by the pineal gland with increased circulating levels shown to inhibit biliary hyperplasia and fibrosis during cholestatic liver injury. Melatonin also has the capability to suppress the release of hypothalamic gonadotropin-releasing hormone (GnRH), a hormone that promotes cholangiocyte proliferation when serum levels are elevated. However, the interplay and contribution of neural melatonin and GnRH to cholangiocyte proliferation and fibrosis in bile duct-ligated (BDL) rats have not been investigated. To test this, cranial levels of melatonin were increased by implanting osmotic minipumps that performed an intracerebroventricular (ICV) infusion of melatonin or saline for 7 days starting at the time of BDL. Hypothalamic GnRH mRNA and cholangiocyte secretion of GnRH and melatonin were assessed. Cholangiocyte proliferation and fibrosis were measured. Primary human hepatic stellate cells (HSCs) were treated with cholangiocyte supernatants, GnRH, or the GnRH receptor antagonist cetrorelix acetate, and cell proliferation and fibrosis gene expression were assessed. Melatonin infusion reduced hypothalamic GnRH mRNA expression and led to decreased GnRH and increased melatonin secretion from cholangiocytes. Infusion of melatonin was found to reduce hepatic injury, cholangiocyte proliferation, and fibrosis during BDL-induced liver injury. HSCs supplemented with BDL cholangiocyte supernatant had increased proliferation, and this increase was reversed when HSCs were supplemented with supernatants from melatonin-infused rats. GnRH stimulated fibrosis gene expression in HSCs, and this was reversed by cetrorelix acetate cotreatment. Increasing bioavailability of melatonin in the brain may improve outcomes during cholestatic liver disease. NEW & NOTEWORTHY We have previously demonstrated that GnRH is expressed in cholangiocytes and promotes their proliferation during cholestasis. In addition, dark therapy, which increases melatonin, reduced cholangiocyte proliferation and fibrosis during cholestasis. This study expands these findings by investigating neural GnRH regulation by melatonin during BDL-induced cholestasis by infusing melatonin into the brain. Melatonin infusion reduced cholangiocyte proliferation and fibrosis, and these effects are due to GNRH receptor 1-dependent paracrine signaling between cholangiocytes and hepatic stellate cells.

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