Evidence map›Paper›PMID 29126263›Full record

ArticleEndocrinology2018

Notch Signaling Regulates Differentiation and Steroidogenesis in Female Mouse Ovarian Granulosa Cells.

Rexxi D Prasasya, Kelly E Mayo

Open 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. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Roles of the Notch Signaling Pathway in Ovarian Functioning.Reproductive sciences (Thousand Oaks, Calif.) · 2021
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Synthesis, Regulatory Factors, and Signaling Pathways of Estrogen in the Ovary.Reproductive sciences (Thousand Oaks, Calif.) · 2023
    Review
  8. Article
  9. Perivascular cells support folliculogenesis in the developing ovary.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Notch signaling in reproduction.Trends in endocrinology and metabolism: TEM · 2021
    Review
  14. Actions and Roles of FSH in Germinative Cells.International journal of molecular sciences · 2021
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
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

2 authors at 1 institution in 1 country.

Rexxi D PrasasyaDepartment of Molecular Biosciences and Center for Reproductive Science, Northwestern University, Evanston, Illinois.
Kelly E MayoDepartment of Molecular Biosciences and Center for Reproductive Science, Northwestern University, Evanston, Illinois.
Northwestern University · US

Funding

Transition Metal Regulation of Oocyte MaturationP01HD021921 · NICHD · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MAYO, KELLY E · 1987 to 2013
$18.5M
CELLULAR &MOLECULAR BASIS OF DISEASE TRAINING PROGRAMT32GM008061 · NIGMS · NORTHWESTERN UNIVERSITY · PI CARTHEW, RICHARD W. · 1985 to 2022
$17.1M
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 P01 HD021921NICHD NIH HHS P50 HD028934NIGMS NIH HHS T32 GM008061
6 · The paper itself

Abstract

The Notch pathway is a highly conserved juxtacrine signaling mechanism that is important for many cellular processes during development, including differentiation and proliferation. Although Notch is important during ovarian follicle formation and early development, its functions during the gonadotropin-dependent stages of follicle development are largely unexplored. We observed positive regulation of Notch activity and expression of Notch ligands and receptors following activation of the luteinizing hormone-receptor in prepubertal mouse ovary. JAG1, the most abundantly expressed Notch ligand in mouse ovary, revealed a striking shift in localization from oocytes to somatic cells following hormone stimulation. Using primary cultures of granulosa cells, we investigated the functions of Jag1 using small interfering RNA knockdown. The loss of JAG1 led to suppression of granulosa cell differentiation as marked by reduced expression of enzymes and factors involved in steroid biosynthesis, and in steroid secretion. Jag1 knockdown also resulted in enhanced cell proliferation. These phenotypes were replicated, although less robustly, following knockdown of the obligate canonical Notch transcription factor RBPJ. Intracellular signaling analysis revealed increased activation of the mitogenic phosphatidylinositol 3-kinase/protein kinase B and mitogen-activated protein kinase/extracellular signal-regulated kinase pathways following Notch knockdown, with a mitogen-activated protein kinase kinase inhibitor blocking the enhanced proliferation observed in Jag1 knockdown granulosa cells. Activation of YB-1, a known regulator of granulosa cell differentiation genes, was suppressed by Jag1 knockdown. Overall, this study reveals a role of Notch signaling in promoting the differentiation of preovulatory granulosa cells, adding to the diverse functions of Notch in the mammalian ovary.

Indexed as

Gene Expression Regulation, DevelopmentalMAP Kinase Signaling SystemAnimalsCell DifferentiationCell ProliferationCells, CulturedChorionic GonadotropinEstradiolFemaleGenes, ReporterGonadotropins, EquineGranulosa CellsGreen Fluorescent ProteinsImmunoglobulin J Recombination Signal Sequence-Binding ProteinJagged-1 ProteinMice, Inbred StrainsChorionic Gonadotropinenhanced green fluorescent proteinEstradiolGonadotropins, EquineGreen Fluorescent ProteinsImmunoglobulin J Recombination Signal Sequence-Binding ProteinJag1 protein, mouseJagged-1 ProteinNotch2 protein, mouseNotch3 protein, mouseProgesteroneRbpj protein, mouseReceptor, Notch2Receptor, Notch3Recombinant Fusion Proteins

Identifiers

PMID29126263
PMCPMC5761600
OpenAlexW2767861043

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.