Evidence map›Paper›PMID 26402718›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2015

Fetal Leydig Cells Persist as an Androgen-Independent Subpopulation in the Postnatal Testis.

Yuichi Shima, Sawako Matsuzaki, Kanako Miyabayashi, Hiroyuki Otake, Takashi Baba, Shigeaki Kato, Ilpo Huhtaniemi, Ken-ichirou Morohashi

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2015. 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
3.3field-weighted citation impact, top 7% 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, 74 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Sertoli cells as a hub in testicular development and male reproductive.Frontiers in cell and developmental biology · 2025
    Review
  7. Article
  8. Review
  9. Article
  10. Fetal Leydig cells: What we know and what we don't.Molecular reproduction and development · 2024
    Review
  11. Article
  12. Intronic Enhancer Is Essential forInternational journal of molecular sciences · 2022
    Article
  13. International journal of molecular sciences · 2022
    Article
  14. Review
  15. Behavior and Functional Roles of CD34International journal of molecular sciences · 2022
    Review
  16. Review
  17. Article
  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

8 authors at 3 institutions in 3 countries.

Yuichi ShimaDepartment of Molecular Biology (Y.S., S.M., K.M., H.O., T.B., K.-i.M.), Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan; Soma Central Hospital (S.K.), Soma, Fukushima 976-0016, Japan; Institute of Reproductive and Developmental Biology (I.H.), Department of Surgery and Cancer, Imperial College London, London W12 0NN, United Kingdom; and Department of Physiology (I.H.), University of Turku, 20520 Turku, Finland.
Sawako MatsuzakiDepartment of Molecular Biology (Y.S., S.M., K.M., H.O., T.B., K.-i.M.), Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan; Soma Central Hospital (S.K.), Soma, Fukushima 976-0016, Japan; Institute of Reproductive and Developmental Biology (I.H.), Department of Surgery and Cancer, Imperial College London, London W12 0NN, United Kingdom; and Department of Physiology (I.H.), University of Turku, 20520 Turku, Finland.
Kanako MiyabayashiDepartment of Molecular Biology (Y.S., S.M., K.M., H.O., T.B., K.-i.M.), Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan; Soma Central Hospital (S.K.), Soma, Fukushima 976-0016, Japan; Institute of Reproductive and Developmental Biology (I.H.), Department of Surgery and Cancer, Imperial College London, London W12 0NN, United Kingdom; and Department of Physiology (I.H.), University of Turku, 20520 Turku, Finland.
Hiroyuki OtakeDepartment of Molecular Biology (Y.S., S.M., K.M., H.O., T.B., K.-i.M.), Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan; Soma Central Hospital (S.K.), Soma, Fukushima 976-0016, Japan; Institute of Reproductive and Developmental Biology (I.H.), Department of Surgery and Cancer, Imperial College London, London W12 0NN, United Kingdom; and Department of Physiology (I.H.), University of Turku, 20520 Turku, Finland.
Takashi BabaDepartment of Molecular Biology (Y.S., S.M., K.M., H.O., T.B., K.-i.M.), Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan; Soma Central Hospital (S.K.), Soma, Fukushima 976-0016, Japan; Institute of Reproductive and Developmental Biology (I.H.), Department of Surgery and Cancer, Imperial College London, London W12 0NN, United Kingdom; and Department of Physiology (I.H.), University of Turku, 20520 Turku, Finland.
Shigeaki KatoDepartment of Molecular Biology (Y.S., S.M., K.M., H.O., T.B., K.-i.M.), Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan; Soma Central Hospital (S.K.), Soma, Fukushima 976-0016, Japan; Institute of Reproductive and Developmental Biology (I.H.), Department of Surgery and Cancer, Imperial College London, London W12 0NN, United Kingdom; and Department of Physiology (I.H.), University of Turku, 20520 Turku, Finland.
Ilpo HuhtaniemiDepartment of Molecular Biology (Y.S., S.M., K.M., H.O., T.B., K.-i.M.), Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan; Soma Central Hospital (S.K.), Soma, Fukushima 976-0016, Japan; Institute of Reproductive and Developmental Biology (I.H.), Department of Surgery and Cancer, Imperial College London, London W12 0NN, United Kingdom; and Department of Physiology (I.H.), University of Turku, 20520 Turku, Finland.
Ken-ichirou MorohashiDepartment of Molecular Biology (Y.S., S.M., K.M., H.O., T.B., K.-i.M.), Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan; Soma Central Hospital (S.K.), Soma, Fukushima 976-0016, Japan; Institute of Reproductive and Developmental Biology (I.H.), Department of Surgery and Cancer, Imperial College London, London W12 0NN, United Kingdom; and Department of Physiology (I.H.), University of Turku, 20520 Turku, Finland.
Kyushu University · JPSoma Central Hospital · JPUniversity of Turku · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Two distinct types of Leydig cells emerge during the development of eutherian mammals. Fetal Leydig cells (FLCs) appear shortly after gonadal sex differentiation, and play a crucial role in masculinization of male fetuses. Meanwhile, adult Leydig cells (ALCs) emerge after birth and induce the secondary male-specific sexual maturation by producing testosterone. Previous histological studies suggested that FLCs regress completely soon after birth. Furthermore, gene disruption studies indicated that androgen signaling is dispensable for FLC differentiation but indispensable for postnatal ALC differentiation. Here, we performed lineage tracing of FLCs using a FLC enhancer of the Ad4BP/SF-1 (Nr5a1) gene and found that FLCs persist in the adult testis. Given that postnatal FLCs expressed androgen receptor (AR) as well as LH receptor (LuR), the effects of AR disruption on FLCs and ALCs were analyzed by crossing AR knockout (KO) mice with FLC-specific enhanced green fluorescent protein (EGFP) mice. Moreover, to eliminate the influence of elevated LH levels in ARKO mice, LuRKO mice and AR/LuR double-KO mice were analyzed. The proportion of ALCs to postnatal FLCs was decreased in ARKO mice, and the effect was augmented in the double-KO mice, suggesting that androgen signaling plays important roles in ALCs, but not in FLCs. Finally, ARKO was achieved in an FLC-specific manner (FLCARKO mice), but the FLC number and gene expression pattern appeared unaffected. These findings support the conclusion that FLCs persist as an androgen-independent Leydig subpopulation in the postnatal testis.

Indexed as

AndrogensAnimalsCell DifferentiationCell LineageEmbryo, MammalianGene Expression Regulation, DevelopmentalGreen Fluorescent ProteinsLeydig CellsMaleMiceMice, Inbred C57BLMice, KnockoutReceptors, AndrogenReceptors, LHSignal TransductionSteroidogenic Factor 1Androgensenhanced green fluorescent proteinGreen Fluorescent ProteinsReceptors, AndrogenReceptors, LHSteroidogenic Factor 1steroidogenic factor 1, mouseTestosterone

Identifiers

PMID26402718
PMCPMC5414671
OpenAlexW2166914736

What OpenQuestion holds

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Registered trials

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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.