Evidence map›Paper›PMID 23125070›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2013

Contribution of Leydig and Sertoli cells to testosterone production in mouse fetal testes.

Yuichi Shima, Kanako Miyabayashi, Shogo Haraguchi, Tatsuhiko Arakawa, Hiroyuki Otake, Takashi Baba, Sawako Matsuzaki, Yurina Shishido, Haruhiko Akiyama, Taro Tachibana and 2 more

Abstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.

0numbers the graph read from it
0cells of the map it votes in
108citing 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

108 citing papers in PubMed, 284 citations in OpenAlex.

  1. Article
  2. Review
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  9. Article
  10. Platelet-derived growth factor receptor alpha regulates fetal testis differentiation via an ERK-CREB axis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  11. Article
  12. Article
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  14. Single-cell resolution uncovers neighboring cell subtypes that share steroidogenic capacity during fetal testis development.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Sertoli cells as a hub in testicular development and male reproductive.Frontiers in cell and developmental biology · 2025
    Review

48 more citing papers are in PubMed but not listed here.

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

12 authors at 4 institutions in 1 country.

Yuichi ShimaDepartment of Molecular Biology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
Kanako Miyabayashi
Shogo Haraguchi
Tatsuhiko Arakawa
Hiroyuki Otake
Takashi Baba
Sawako Matsuzaki
Yurina Shishido
Haruhiko Akiyama
Taro Tachibana
Kazuyoshi Tsutsui
Ken-ichirou Morohashi
Kyushu University · JPOsaka City University · JPWaseda University · JPKyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Testosterone is a final product of androgenic hormone biosynthesis, and Leydig cells are known to be the primary source of androgens. In the mammalian testis, two distinct populations of Leydig cells, the fetal and the adult Leydig cells, develop sequentially, and these two cell types differ both morphologically and functionally. It is well known that the adult Leydig cells maintain male reproductive function by producing testosterone. However, it has been controversial whether fetal Leydig cells can produce testosterone, and the synthetic pathway of testosterone in the fetal testis is not fully understood. In the present study, we generated transgenic mice in which enhanced green fluorescence protein was expressed under the control of a fetal Leydig cell-specific enhancer of the Ad4BP/SF-1 (Nr5a1) gene. The transgene construct was prepared by mutating the LIM homeodomain transcription factor (LHX9)-binding sequence in the promoter, which abolished promoter activity in the undifferentiated testicular cells. These transgenic mice were used to collect highly pure fetal Leydig cells. Gene expression and steroidogenic enzyme activities in the fetal Leydig cells as well as in the fetal Sertoli cells and adult Leydig cells were analyzed. Our results revealed that the fetal Leydig cells synthesize only androstenedione because they lack expression of Hsd17b3, and fetal Sertoli cells convert androstenedione to testosterone, whereas adult Leydig cells synthesize testosterone by themselves. The current study demonstrated that both Leydig and Sertoli cells are required for testosterone synthesis in the mouse fetal testis.

Indexed as

AnimalsBase SequenceBinding SitesCells, CulturedConserved SequenceFetusGene ExpressionGene Expression RegulationGenes, ReporterGreen Fluorescent ProteinsLeydig CellsMaleMiceMice, TransgenicMolecular Sequence DataPromoter Regions, Geneticenhanced green fluorescent proteinGreen Fluorescent ProteinsSteroidogenic Factor 1Testosterone

Identifiers

PMID23125070
PMCPMC5416943
OpenAlexW2003004843

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.