Evidence map›Paper›PMID 21700720›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2011

Impaired FSHbeta expression in the pituitaries of Foxl2 mutant animals.

Nicholas J Justice, Amy L Blount, Emanuele Pelosi, David Schlessinger, Wylie Vale, Louise M Bilezikjian

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  6. Expression ofAnimals : an open access journal from MDPI · 2019
    Article
  7. Review
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  10. Review
  11. Genetic regulation of murine pituitary development.Journal of molecular endocrinology · 2015
    Review
  12. Article
  13. Article
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  15. Follicle-stimulating hormone synthesis and fertility are intact in mice lacking SMAD3 DNA binding activity and SMAD2 in gonadotrope cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014
    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

6 authors at 2 institutions in 1 country.

Nicholas J JusticeClayton Foundation Laboratories for Peptide Biology, Salk Institute for Biological Studies, La Jolla, California 92037, USA.
Amy L Blount
Emanuele Pelosi
David Schlessinger
Wylie Vale
Louise M Bilezikjian
Salk Institute for Biological Studies · USNational Institute on Aging · US

Funding

Genes Associated With Ovarian Development and Premature Ovarian Failure - testZIAAG000647 · NIA · NATIONAL INSTITUTE ON AGING · PI SCHLESSINGER, DAVID · 2009 to 2017
$6.2M
Regulation of Follistatin Expression by ActivinR01HD046941 · NICHD · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI BILEZIKJIAN, LOUISE M · 2004 to 2014
$3.5M
Intramural NIH HHSNICHD NIH HHS 2R01HD046941NICHD NIH HHS R01 HD046941
6 · The paper itself

Abstract

Forkhead box L2 (FoxL2) is required for ovarian development and differentiation. FoxL2 is also expressed in the pituitary where it has been implicated in the development and regulation of gonadotropes, which secrete LH and FSH, the endocrine signals that regulate folliculogenesis in the ovary and spermatogenesis in the testis. Here, we show that FoxL2 is not required for the specification of gonadotropes; the pituitaries of Foxl2 mutant mice contain normal numbers of gonadotropes that express glycoprotein α subunit and LHβ. Whereas the specification of gonadotropes and all other hormonal cell types is normal in the pituitaries of Foxl2 mutant animals, FSHβ levels are severely impaired in both male and female animals, suggesting that FoxL2 is required for normal Fshb expression. The size of the pituitary is reduced in proportion to the smaller body size of Foxl2 mutants, with a concomitant increase in the pituitary cellular density. In primary pituitary cultures, activin induces FSH secretion and Fshb mRNA expression in cells from wild-type mice. In cells from Foxl2 mutant mice, however, FSH secretion is not detected, and activin is unable to drive Fshb expression, suggesting that the mechanism of activin-dependent activation of Fshb transcription is impaired. However, a small number of gonadotropes in the ventromedial region of the pituitaries from Foxl2 mutant mice maintain FSHβ expression, suggesting that a FoxL2- and activin-independent mechanism can drive Fshb transcription. These data indicate that, in addition to its role in the ovary, FoxL2 function in the pituitary is required for normal expression of FSH.

Indexed as

Activin ReceptorsActivinsAnimalsCell CountCells, CulturedFemaleFollicle Stimulating Hormone, beta SubunitForkhead Box Protein L2Forkhead Transcription FactorsGene Expression RegulationGonadotrophsLuteinizing HormoneMaleMiceMice, Inbred C57BLMice, Mutant StrainsActivin ReceptorsActivinsFollicle Stimulating Hormone, beta SubunitForkhead Box Protein L2Forkhead Transcription FactorsFoxl2 protein, mouseLuteinizing HormoneRNA, MessengerSmad Proteins

Identifiers

PMID21700720
PMCPMC3146251
OpenAlexW1989579011

What OpenQuestion holds

Textmetadata
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.