Evidence map›Paper›PMID 34725674›Full record

ArticleBiology of reproduction2022

Regulation of mouse primordial follicle formation by signaling through the PI3K pathway†.

Joshua J N Burton, Amanda J Luke, Melissa E Pepling

Open access · greenAbstract read
In one paragraph

Article in Biology of reproduction, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Building a resilient ovarian reserve: Early soma-oocyte interactions.Current topics in developmental biology · 2026
    Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Epigenetic programming in the ovarian reserve.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023
    Article
  15. Steroidogenic factor 1 (SF-1;Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Maternal pre-conceptional glyphosate exposure impacts the offspring hepatic and ovarian proteome.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article
  17. Current progress onFrontiers in cell and developmental biology · 2023
    Review
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

3 authors at 1 institution in 1 country.

Joshua J N BurtonDepartment of Biology, Syracuse University, Syracuse, NY, USA.
Amanda J LukeDepartment of Biology, Syracuse University, Syracuse, NY, USA.
Melissa E PeplingDepartment of Biology, Syracuse University, Syracuse, NY, USA.
Syracuse University · US

Funding

Regulation of Primordial Follicle Formation and Oocyte SurvivalR15HD075257 · NICHD · SYRACUSE UNIVERSITY · PI PEPLING, MELISSA E · 2015 to 2015
$440k
NICHD NIH HHS R15 HD075257
6 · The paper itself

Abstract

Cell signaling mediated by the KIT receptor is critical for many aspects of oogenesis including the proliferation and migration of primordial germ cells, as well as the survival, growth, and maturation of ovarian follicles. We previously showed that KIT regulates cyst breakdown and primordial follicle formation, and in this study, have investigated the mechanisms downstream of the receptor by modulating the activity of two downstream signaling cascades: the phosphoinositide 3-kinase (PI3K) and the mitogen-activated protein kinase pathways. E17.5 ovaries were cultured for 5 days with a daily dose of media supplemented with either the PI3K inhibitor LY294002, the MEK inhibitor U0126, or a DMSO vehicle control. Our histological observations aligned with the established role of PI3K in oocyte growth and primordial follicle activation but also revealed that LY294002 treatment delayed the processes of cyst breakdown and primordial follicle formation. U0126 treatment also led to a reduction in oocyte growth and follicle development but did not appear to affect cyst breakdown. The delay in cyst breakdown was mitigated when ovaries were dually dosed with LY294002 and KITL, suggesting that while KIT may signal through PI3K to promote cyst breakdown, other signaling networks downstream of the receptor could compensate. These observations unearth a role for PI3K signaling in the establishment of the ovarian reserve and suggest that PI3K might be the primary mediator of KIT-induced cyst breakdown and primordial follicle formation in the mouse ovary.

Indexed as

CystsPhosphatidylinositol 3-KinasesAnimalsFemaleMiceOocytesOvarian FolliclePhosphatidylinositol 3-KinaseSignal TransductionPhosphatidylinositol 3-KinasePhosphatidylinositol 3-Kinasescyst breakdownoocyte growthPI3K signalingprimordial follicle formation

Identifiers

PMID34725674
PMCPMC8934696
OpenAlexW3208347687

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.