Evidence map›Paper›PMID 30364975›Full record

ArticleEndocrinology2018

Betaglycan (TGFBR3) Functions as an Inhibin A, but Not Inhibin B, Coreceptor in Pituitary Gonadotrope Cells in Mice.

Yining Li, Jérôme Fortin, Luisina Ongaro, Xiang Zhou, Ulrich Boehm, Alan Schneyer, Daniel J Bernard, Herbert Y Lin

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.4field-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

32 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
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  10. Synthesis ofOrganic & biomolecular chemistry · 2023
    Article
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  20. TGF-β superfamily co-receptors in cancer.Developmental dynamics : an official publication of the American Association of Anatomists · 2022
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 3 countries.

Yining LiDepartment of Pharmacology and Therapeutics, McGill University, Montréal, Québec, Canada.
Jérôme FortinDepartment of Pharmacology and Therapeutics, McGill University, Montréal, Québec, Canada.
Luisina OngaroDepartment of Pharmacology and Therapeutics, McGill University, Montréal, Québec, Canada.
Xiang ZhouDepartment of Pharmacology and Therapeutics, McGill University, Montréal, Québec, Canada.
Ulrich BoehmDepartment of Pharmacology and Toxicology, University of Saarland School of Medicine, Homburg, Germany.
Alan SchneyerFairbanks Pharmaceuticals, Concord, Massachusetts.
Daniel J BernardDepartment of Pharmacology and Therapeutics, McGill University, Montréal, Québec, Canada.
Herbert Y LinProgram in Membrane Biology/Nephrology, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.
McGill University · CAHarvard University · USSaarland University · DE

Funding

Testosterone-GnRH Frequency and the Evolution of PCOS in AdolescenceP50HD028934 · NICHD · UNIVERSITY OF VIRGINIA · PI HAISENLEDER, DANIEL J. · 2014 to 2018
$8.6M
NICHD NIH HHS P50 HD028934
6 · The paper itself

Abstract

Inhibins are gonadal hormones that act on pituitary gonadotrope cells to suppress FSH synthesis and secretion. Inhibin A and B are heterodimers of the inhibin ⍺-subunit disulfide-linked to one of two inhibin β-subunits. Homodimers or heterodimers of the inhibin β-subunits form the activins, which stimulate FSH production. Activins signal through complexes of type I and II receptor serine/threonine kinases to increase transcription of the FSHβ subunit gene. According to in vitro observations, inhibins impair FSH synthesis by competitively binding to activin type II receptors, particularly in the presence of the TGFβ type III receptor (TGFBR3, or betaglycan). The role of TGFBR3 in inhibin action in vivo has not been determined. Here, we ablated Tgfbr3 specifically in murine gonadotropes. Conditional knockout females were supra-fertile, exhibiting enhanced folliculogenesis, numbers of ovulated eggs per cycle, and litter sizes relative to control mice. Despite these phenotypes, FSH levels appeared to be unaltered in knockout mice, and the mechanisms underlying their enhanced fertility remain unexplained. Inhibin B is the predominant form of the hormone in males and in females during most stages of the estrous cycle. Remarkably, inhibin A, but not inhibin B, suppression of FSH synthesis was impaired in cultured pituitaries of knockout mice, which may explain the absence of discernible changes in FSH levels in vivo. Collectively, these data challenge current dogma by demonstrating that TGFBR3 (betaglycan) functions as an inhibin A, but not an inhibin B, coreceptor in gonadotrope cells in vivo. Mechanisms of inhibin B action merit further investigation.

Indexed as

AnimalsCells, CulturedEmbryo, MammalianFemaleFertilityFollicle Stimulating HormoneGonadotrophsInhibinsMaleMiceMice, Inbred C57BLMice, KnockoutPregnancyProtein BindingProtein MultimerizationProteoglycansbetaglycanFollicle Stimulating Hormoneinhibin Ainhibin BInhibinsProteoglycansReceptors, Transforming Growth Factor beta

Identifiers

PMID30364975
PMCPMC6372943
OpenAlexW2898505007

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.