Evidence map›Paper›PMID 27569529›Full record

ArticleMolecular and cellular endocrinology2016

The relationship between basal and regulated Gnrhr expression in rodent pituitary gonadotrophs.

Ivana Bjelobaba, Marija M Janjic, Jovana S Tavcar, Marek Kucka, Melanija Tomić, Stanko S Stojilkovic

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 13 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Ivana BjelobabaSection on Cellular Signaling, Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, MD 20892-4510, United States.
Marija M JanjicSection on Cellular Signaling, Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, MD 20892-4510, United States.
Jovana S TavcarSection on Cellular Signaling, Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, MD 20892-4510, United States.
Marek KuckaSection on Cellular Signaling, Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, MD 20892-4510, United States.
Melanija TomićSection on Cellular Signaling, Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, MD 20892-4510, United States.
Stanko S StojilkovicSection on Cellular Signaling, Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, MD 20892-4510, United States. Electronic address: stojilks@mail.nih.gov.
Eunice Kennedy Shriver National Institute of Child Health and Human Development · US

Funding

Intracellular Signaling In Endocrine CellsZIAHD000195 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI STOJILKOVIC, STANKO S. · 2009 to 2025
$18.8M
Intramural NIH HHS ZIA HD000195
6 · The paper itself

Abstract

Hypothalamic GnRH together with gonadal steroids and activins/inhibin regulate its receptor gene (Gnrhr) expression in vivo, which leads to crucial changes in GnRHR numbers on the plasma membrane. This is accompanied by alterations in the gonadotroph sensitivity and responsiveness during physiologically relevant situations. Here we investigated basal and GnRH-regulated Gnrhr expression in rodent pituitary gonadotrophs in vitro. In pituitary cells from adult animals cultured in the absence of GnRH and steroid hormones, the Gnrhr expression was progressively reduced but not completely abolished. The basal Gnrhr expression was also operative in LβT2 immortalized gonadotrophs never exposed to GnRH. In both cell types, basal transcription was sufficient for the expression of functional GnRHRs. Continuous application of GnRH transiently elevated the Gnrhr expression in cultured pituitary cells followed by a sustained fall without affecting basal transcription. Both basal and regulated Gnrhr transcriptions were dependent on the protein kinase C signaling pathway. The GnRH-regulated Gnrhr expression was not operative in embryonal pituitary and LβT2 cells and was established neonatally, the sex-specific response patterns were formed at the juvenile-peripubertal stage and there was a strong correlation between basal and regulated gene expression during development. Thus, the age-dependent basal and regulated Gnrhr transcription could account for the initial blockade and subsequent activation of the reproductive system during development.

Indexed as

Gene Expression RegulationAnimalsCalciumCell Line, TransformedCyclic AMPDown-RegulationFemaleGonadotrophsMaleMAP Kinase Signaling SystemProtein Kinase CRats, Sprague-DawleyReceptors, LHRHTetradecanoylphorbol AcetateTranscription, GeneticUp-RegulationCalciumCyclic AMPProtein Kinase CReceptors, LHRHTetradecanoylphorbol AcetateERK1/2GnRHGnrhrGonadotrophsLβT2 cellsProtein kinase C

Identifiers

PMID27569529
PMCPMC6364298
OpenAlexW2514337843

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.