Evidence map›Paper›PMID 17138645›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2007

Reciprocal cross talk between gonadotropin-releasing hormone (GnRH) and prostaglandin receptors regulates GnRH receptor expression and differential gonadotropin secretion.

Zvi Naor, Henry N Jabbour, Michal Naidich, Adam J Pawson, Kevin Morgan, Sharon Battersby, Michael R Millar, Pamela Brown, Robert P Millar

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

15 citing papers in PubMed, 54 citations in OpenAlex.

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  9. Review
  10. β-catenin regulates GnRH-induced FSHβ gene expression.Molecular endocrinology (Baltimore, Md.) · 2013
    Article
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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

9 authors at 4 institutions in 2 countries.

Zvi NaorMedical Research Council (MRC), Huamn Reproduction Sciences, Centre for Reproductive Biology, The Queen's Medical Research Institute, Edinburgh, United Kingdom. zvin@tauex.tau.ac.il
Henry N Jabbour
Michal Naidich
Adam J Pawson
Kevin Morgan
Sharon Battersby
Michael R Millar
Pamela Brown
Robert P Millar
Medical Research Council · GBMRC Centre for Reproductive Health · GBTel Aviv University · ILThe Queen's Medical Research Institute · GB

Funding

Medical Research Council MC_U127681325Medical Research Council MC_U127684438Medical Research Council MC_U127684446Medical Research Council MC_U127685842Medical Research Council U.1276.00.004.00002.01/2(61014)Medical Research Council U.1276.00.005.00002.01 (85842)Medical Research Council U.1276.00.005(61049)
6 · The paper itself

Abstract

The asynchronous secretion of gonadotrope LH and FSH under the control of GnRH is crucial for ovarian cyclicity but the underlying mechanism is not fully resolved. Because prostaglandins (PG) are autocrine regulators in many tissues, we determined whether they have this role in gonadotropes. We first demonstrated that GnRH stimulates PG synthesis by induction of cyclooxygenase-2, via the protein kinase C/c-Src/phosphatidylinositol 3'-kinase/MAPK pathway in the LbetaT2 gonadotrope cell line. We then demonstrated that PGF(2alpha) and PGI2, but not PGE2 inhibited GnRH receptor expression by inhibition of phosphoinositide turnover. PGF(2alpha), but not PGI2 or PGE2, reduced GnRH-induction of LHbeta gene expression, but not the alpha-gonadotropin subunit or the FSHbeta subunit genes. The prostanoid receptors EP1, EP2, FP, and IP were expressed in rat gonadotropes. Incubations of rat pituitaries with PGF(2alpha), but not PGI2 or PGE2, inhibited GnRH-induced LH secretion, whereas the cyclooxygenase inhibitor, indomethacin, stimulated GnRH-induced LH secretion. None of these treatments had any effect on GnRH-induced FSH secretion. The findings have thus elaborated a novel GnRH signaling pathway mediated by PGF(2alpha)-FP and PGI2-IP, which acts through an autocrine/paracrine modality to limit autoregulation of the GnRH receptor and differentially inhibit LH and FSH release. These findings provide a mechanism for asynchronous LH and FSH secretions and suggest the use of combination therapies of GnRH and prostanoid analogs to treat infertility, diseases with unbalanced LH and FSH secretion and in hormone-dependent diseases such as prostatic cancer.

Indexed as

AnimalsCell LineCSK Tyrosine-Protein KinaseCyclooxygenase 2Cyclooxygenase InhibitorsEnzyme InductionFollicle Stimulating HormoneFollicle Stimulating Hormone, beta SubunitGene Expression RegulationGonadotropin-Releasing HormoneIndomethacinIn Vitro TechniquesLuteinizing HormoneMAP Kinase Signaling SystemPhosphatidylinositol 3-KinasesPhosphatidylinositolsCSK Tyrosine-Protein KinaseCyclooxygenase 2Cyclooxygenase InhibitorsFollicle Stimulating HormoneFollicle Stimulating Hormone, beta SubunitGonadotropin-Releasing HormoneIndomethacinLuteinizing HormonePhosphatidylinositol 3-KinasesPhosphatidylinositolsProstaglandinsProtein Kinase CProtein-Tyrosine KinasesReceptors, LHRHReceptors, Prostaglandinsrc-Family Kinases

Identifiers

PMID17138645
PMCPMC1951794
OpenAlexW2138968161

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.