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Regulation of rat ovarian gonadotropin Releasing hormone receptor mRNA levels Väänänen, Céline Claire Magali
Abstract
The studies undertaken herewithin sought to characterize the pattern of regulation of the gonadotrophin-releasing hormone receptor (GnRH-R) mRNA levels in the rat ovary. The demonstration of gonadotrophin-releasing hormone (GnRH) transcripts in steroidproducing and steroid-dependent tissues suggests that GnRH may be implicated in the modulation of steroid action in those target tissues. Expression of GnRH-R mRNA increases in gonadal tissues and the pituitary with age, supporting the concept of GnRH as a local regulator in the developing rat as well as in the adult. During the peri-ovulatory period, stimulation of the ovarian luteinizing hormone receptor (LH-R) by an ovulatory dose of human chorionic gonadotrophin (hCG) is capable of inducing a transient and pronounced decrease in GnRH-R mRNA levels, thus bringing more evidence to the role of GnRH in the regulation of ovarian function during ovulation. The gene encoding GnRH-R was found to be expressed in granulosa cells. In a follicle stimulating hormone (FSH) pre-treated granulosa cell model, GnRH-R gene transcript levels were negatively influenced by LH, but not FSH, in a time- and concentration-dependent manner. Autostimulation of GnRH-R by GnRH was also seen. In a second granulosa cell model obtained from pregnant mare serum gonadotrophin (PMSG) synchronized immature rats, the levels of GnRH-R transcripts were found to be positively regulated by hCG and GnRH, while prostaglandin F2a (PGF20;) inhibited GnRH-R mRNA levels in a bell curve-like fashion. However, combinations of these treatments canceled each other's effects. In this model, GnRH stimulated progesterone (P4) production and only slightly inhibited hCG-stimulated progesterone production. This modulation in the responses to GnRH and in the levels of GnRH-R mRNA suggest that GnRH may have different actions at different times of follicular development. In conclusion, the findings of the present study demonstrate wide spread expression of the GnRH-R gene in steroidogenic or steroid-dependent tissues. Gonadotrophin-releasing hormone receptor mRNA levels were shown to be regulated by gonadotrophins, PGF2a and GnRH in the whole ovary and in granulosa cells, strongly supporting the postulated role of GnRH-R in the local modulations of ovarian function mediated by GnRH.
Item Metadata
Title |
Regulation of rat ovarian gonadotropin Releasing hormone receptor mRNA levels
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Creator | |
Publisher |
University of British Columbia
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Date Issued |
1997
|
Description |
The studies undertaken herewithin sought to characterize the pattern of regulation of the
gonadotrophin-releasing hormone receptor (GnRH-R) mRNA levels in the rat ovary.
The demonstration of gonadotrophin-releasing hormone (GnRH) transcripts in steroidproducing
and steroid-dependent tissues suggests that GnRH may be implicated in the modulation
of steroid action in those target tissues. Expression of GnRH-R mRNA increases in gonadal
tissues and the pituitary with age, supporting the concept of GnRH as a local regulator in the
developing rat as well as in the adult.
During the peri-ovulatory period, stimulation of the ovarian luteinizing hormone receptor
(LH-R) by an ovulatory dose of human chorionic gonadotrophin (hCG) is capable of inducing a
transient and pronounced decrease in GnRH-R mRNA levels, thus bringing more evidence to the
role of GnRH in the regulation of ovarian function during ovulation.
The gene encoding GnRH-R was found to be expressed in granulosa cells. In a follicle
stimulating hormone (FSH) pre-treated granulosa cell model, GnRH-R gene transcript levels were
negatively influenced by LH, but not FSH, in a time- and concentration-dependent manner. Autostimulation
of GnRH-R by GnRH was also seen. In a second granulosa cell model obtained from
pregnant mare serum gonadotrophin (PMSG) synchronized immature rats, the levels of GnRH-R
transcripts were found to be positively regulated by hCG and GnRH, while prostaglandin F2a
(PGF20;) inhibited GnRH-R mRNA levels in a bell curve-like fashion. However, combinations of
these treatments canceled each other's effects. In this model, GnRH stimulated progesterone (P4)
production and only slightly inhibited hCG-stimulated progesterone production. This modulation
in the responses to GnRH and in the levels of GnRH-R mRNA suggest that GnRH may have
different actions at different times of follicular development.
In conclusion, the findings of the present study demonstrate wide spread expression of the
GnRH-R gene in steroidogenic or steroid-dependent tissues. Gonadotrophin-releasing hormone
receptor mRNA levels were shown to be regulated by gonadotrophins, PGF2a and GnRH in the
whole ovary and in granulosa cells, strongly supporting the postulated role of GnRH-R in the local
modulations of ovarian function mediated by GnRH.
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Extent |
15192899 bytes
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Genre | |
Type | |
File Format |
application/pdf
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Language |
eng
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Date Available |
2009-03-27
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Provider |
Vancouver : University of British Columbia Library
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Rights |
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.
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DOI |
10.14288/1.0088002
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URI | |
Degree | |
Program | |
Affiliation | |
Degree Grantor |
University of British Columbia
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Graduation Date |
1997-05
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Campus | |
Scholarly Level |
Graduate
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Aggregated Source Repository |
DSpace
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Rights
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.