Evidence map›Paper›PMID 28051360›Full record

ArticleStem cells and development2017

The NOTCH Ligand JAG1 Regulates GDNF Expression in Sertoli Cells.

Thomas X Garcia, Parag Parekh, Pooja Gandhi, Krishna Sinha, Marie-Claude Hofmann

Abstract read
In one paragraph

Article in Stem cells and development, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

38 citing papers in PubMed, 68 citations in OpenAlex.

  1. Role of Estrogen Signaling in Notch Pathway Activation in Sertoli Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2025
    Article
  2. Article
  3. Sertoli cells as a hub in testicular development and male reproductive.Frontiers in cell and developmental biology · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Transcriptional profiling of β-2MStem cell reports · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  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

5 authors at 1 institution in 1 country.

Thomas X Garcia1 Department of Endocrine Neoplasia and Hormonal Disorders, University of Texas, MD Anderson Cancer Center , Houston, Texas.
Parag Parekh1 Department of Endocrine Neoplasia and Hormonal Disorders, University of Texas, MD Anderson Cancer Center , Houston, Texas.
Pooja Gandhi1 Department of Endocrine Neoplasia and Hormonal Disorders, University of Texas, MD Anderson Cancer Center , Houston, Texas.
Krishna Sinha1 Department of Endocrine Neoplasia and Hormonal Disorders, University of Texas, MD Anderson Cancer Center , Houston, Texas.
Marie-Claude Hofmann1 Department of Endocrine Neoplasia and Hormonal Disorders, University of Texas, MD Anderson Cancer Center , Houston, Texas.
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Molecular Regulation of the Perinatal Male Germ Cell NicheR01HD081244 · NICHD · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HOFMANN, MARIE-CLAUDE CATHERINE · 2014 to 2018
$1.6M
NCI NIH HHS P30 CA016672NICHD NIH HHS R01 HD081244
6 · The paper itself

Abstract

In the seminiferous epithelium of the testis, Sertoli cells are key niche cells directing proliferation and differentiation of spermatogonial stem cells (SSCs) into spermatozoa. Sertoli cells produce glial cell line-derived neurotrophic factor (GDNF), which is essential for SSC self-renewal and progenitor expansion. While the role of GDNF in the testis stem cell niche is established, little is known about how this factor is regulated. Our previous studies on NOTCH activity in Sertoli cells demonstrated a role of this pathway in limiting stem/progenitor cell numbers, thus ultimately downregulating sperm cell output. In this study we demonstrate through a double-mutant mouse model that NOTCH signaling in Sertoli cells functions solely through the canonical pathway. Further, we demonstrate through Dual luciferase assay and chromatin immunoprecipitation quantitative polymerase chain reaction (ChIP-qPCR) analysis that the NOTCH targets HES1 and HEY1, which are transcriptional repressors, directly downregulate GDNF expression by binding to the Gdnf promoter, thus antagonizing the effects of FSH/cAMP. Finally, we demonstrate that testicular stem/progenitors cells are activating NOTCH signaling in Sertoli cells in vivo and in vitro through the NOTCH ligand JAG1 at their surface, indicating that these cells may ensure their own homeostasis through negative feedback regulation.

Indexed as

Signal TransductionSpermatogenesisAnimalsCell Cycle ProteinsCells, CulturedCyclic AMPFeedback, PhysiologicalGlial Cell Line-Derived Neurotrophic FactorJagged-1 ProteinMaleMicePromoter Regions, GeneticReceptors, NotchSertoli CellsSpermatogoniaStem Cell NicheCell Cycle ProteinsCyclic AMPGlial Cell Line-Derived Neurotrophic FactorHes1 protein, mouseHey1 protein, mouseJag1 protein, mouseJagged-1 ProteinReceptors, NotchTranscription Factor HES-1GDNFJAG1NOTCHSertoli cellspermatogenesisspermatogonia

Identifiers

PMID28051360
PMCPMC5393414
OpenAlexW2570104463

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.