Front Endocrinol (Lausanne). 2017 Sep 4;8:221. doi: 10.3389/fendo.2017.00221. eCollection 2017.
Intrinsic and Regulated Gonadotropin-Releasing Hormone Receptor Gene Transcription in Mammalian Pituitary Gonadotrophs.
Abstract
The hypothalamic decapeptide gonadotropin-releasing hormone (GnRH), acting via its receptors (GnRHRs) expressed in pituitary
gonadotrophs, represents a critical molecule in control of reproductive
functions in all vertebrate species. GnRH-activated receptors regulate
synthesis of gonadotropins in a frequency-dependent manner. The number
of GnRHRs on the plasma membrane determines the responsiveness of
gonadotrophs to GnRH and varies in relation to age, sex, and
physiological status. This is achieved by a complex control that
operates at transcriptional, translational, and posttranslational
levels. This review aims to overview the mechanisms of GnRHR gene (Gnrhr) transcription in mammalian gonadotrophs.
In general, Gnrhr exhibits basal and regulated transcription activities. Basal Gnrhr transcription appears to be an intrinsic property of native and immortalized gonadotrophs that secures the presence of a sufficient number GnRHRs to preserve their functionality independently of the status of regulated transcription.
On the other hand, regulated transcription modulates GnRHR expression during development, reproductive cycle, and aging.
GnRH is crucial for regulated Gnrhr transcription in native gonadotrophs but is ineffective in immortalized gonadotrophs.
In rat and mouse, both basal and GnRH-induced Gnrhr transcription rely primarily on the protein kinase C signaling pathway, with subsequent activation of mitogen-activated protein kinases.
Continuous GnRH application, after a transient stimulation, shuts off regulated but not basal transcription, suggesting that different branches of this signaling pathway control transcription. Pituitary adenylate cyclase-activating polypeptide (PACAP) , but not activins, contributes to the regulated transcription utilizing the protein kinase A (PKA) signaling pathway, whereas a mechanisms by which steroid hormones modulate Gnrhr transcription has not been well characterized.
In general, Gnrhr exhibits basal and regulated transcription activities. Basal Gnrhr transcription appears to be an intrinsic property of native and immortalized gonadotrophs that secures the presence of a sufficient number GnRHRs to preserve their functionality independently of the status of regulated transcription.
On the other hand, regulated transcription modulates GnRHR expression during development, reproductive cycle, and aging.
GnRH is crucial for regulated Gnrhr transcription in native gonadotrophs but is ineffective in immortalized gonadotrophs.
In rat and mouse, both basal and GnRH-induced Gnrhr transcription rely primarily on the protein kinase C signaling pathway, with subsequent activation of mitogen-activated protein kinases.
Continuous GnRH application, after a transient stimulation, shuts off regulated but not basal transcription, suggesting that different branches of this signaling pathway control transcription. Pituitary adenylate cyclase-activating polypeptide (PACAP) , but not activins, contributes to the regulated transcription utilizing the protein kinase A (PKA) signaling pathway, whereas a mechanisms by which steroid hormones modulate Gnrhr transcription has not been well characterized.
KEYWORDS:
basal transcription; gonadotrophs; gonadotropin-releasing hormone; gonadotropin-releasing hormone receptor; regulated transcription20.1. 2018 Pohdittavaksi tämä monimutkainen feed back järjestelmä.
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