Evidence map›Paper›PMID 25140527›Full record

ArticlePloS one2014

Transforming growth factor-β1 signaling represses testicular steroidogenesis through cross-talk with orphan nuclear receptor Nur77.

Eunsook Park, Chin-Hee Song, Jae-Il Park, Ryun-Sup Ahn, Hueng-Sik Choi, CheMyong Ko, Keesook Lee

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  5. Biomolecules · 2025
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  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Signaling by TGF-betas in tubule cultures of adult rat testis.American journal of translational research · 2017
    Article
  13. 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

7 authors at 4 institutions in 2 countries.

Eunsook ParkHormone Research Center, School of Biological Sciences and Technology, Chonnam National University, Gwangju, Republic of Korea.
Chin-Hee SongHormone Research Center, School of Biological Sciences and Technology, Chonnam National University, Gwangju, Republic of Korea.
Jae-Il ParkKorea Basic Science Institute, Gwangju Center at Chonnam National University, Gwangju, Republic of Korea.
Ryun-Sup AhnGraduate School of Integrative Medicine, CHA Medical University, Seoul, Republic of Korea.
Hueng-Sik ChoiHormone Research Center, School of Biological Sciences and Technology, Chonnam National University, Gwangju, Republic of Korea.
CheMyong KoDepartment of Comparative Biosciences, College of Veterinary Medicine, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.
Keesook LeeHormone Research Center, School of Biological Sciences and Technology, Chonnam National University, Gwangju, Republic of Korea.
Chonnam National University · KRCHA University · KRKorea Basic Science Institute · KRUniversity of Illinois Urbana-Champaign · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor- β1 (TGF-β1) has been reported to inhibit luteinizing hormone (LH) mediated-steroidogenesis in testicular Leydig cells. However, the mechanism by which TGF-β1 controls the steroidogenesis in Leydig cells is not well understood. Here, we investigated the possibility that TGF-β1 represses steroidogenesis through cross-talk with the orphan nuclear receptor Nur77. Nur77, which is induced by LH/cAMP signaling, is one of major transcription factors that regulate the expression of steroidogenic genes in Leydig cells. TGF-β1 signaling inhibited cAMP-induced testosterone production and the expression of steroidogenic genes such as P450c17, StAR and 3β-HSD in mouse Leydig cells. Further, TGF-β1/ALK5 signaling repressed cAMP-induced and Nur77-activated promoter activity of steroidogenic genes. In addition, TGF-β1/ALK5-activated Smad3 repressed Nur77 transactivation of steroidogenic gene promoters by interfering with Nur77 binding to DNA. In primary Leydig cells isolated from Tgfbr2flox/flox Cyp17iCre mice, TGF-β1-mediated repression of cAMP-induced steroidogenic gene expression was significantly less than that in primary Leydig cells from Tgfbr2flox/flox mice. Taken together, these results suggest that TGF-β1/ALK5/Smad3 signaling represses the expression of steroidogenic genes via the suppression of Nur77 transactivation in testicular Leydig cells. These findings may provide a molecular mechanism involved in the TGF-β1-mediated repression of testicular steroidogenesis.

Indexed as

3-Hydroxysteroid DehydrogenasesAnimalsCyclic AMPGene Expression Regulation, EnzymologicLeydig CellsMaleMiceNuclear Receptor Subfamily 4, Group A, Member 1PhosphoproteinsPromoter Regions, GeneticSignal TransductionSmad3 ProteinSteroid 17-alpha-HydroxylaseSteroidogenic Acute Regulatory ProteinTestisTestosterone3-Hydroxysteroid DehydrogenasesCyclic AMPNuclear Receptor Subfamily 4, Group A, Member 1PhosphoproteinsSmad3 ProteinSteroid 17-alpha-HydroxylaseSteroidogenic Acute Regulatory ProteinTestosteroneTransforming Growth Factor beta1

Identifiers

PMID25140527
PMCPMC4139307
OpenAlexW1982662530

What OpenQuestion holds

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LicenceCC BY
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.