Evidence map›Paper›PMID 41436489›Full record

ArticleScientific reports2025

RU 486 blocks inhibitory effect of neonatal corticosterone administration on sertoli cell proliferation in mice.

Hidenobu Miyaso, Yutaro Natsuyama, Shinichi Kawata, Tomiko Yakura, Zhong-Lian Li, Miyuki Kuramasu, Shota Tanifuji, Xi Wu, Yuki Ogawa, Yoshiharu Matsuno and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Hidenobu MiyasoDepartment of Anatomy, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, 160-8402, Tokyo, Japan. miyaso.hidenobu.6b@tokyo-med.ac.jp.
Yutaro NatsuyamaDepartment of Anatomy, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, 160-8402, Tokyo, Japan.
Shinichi KawataDepartment of Anatomy, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, 160-8402, Tokyo, Japan.
Tomiko YakuraDepartment of Anatomy, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, 160-8402, Tokyo, Japan.
Zhong-Lian LiDepartment of Anatomy, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, 160-8402, Tokyo, Japan.
Miyuki KuramasuDepartment of Anatomy, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, 160-8402, Tokyo, Japan.
Shota TanifujiDepartment of Anatomy, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, 160-8402, Tokyo, Japan.
Xi WuDepartment of Anatomy, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, 160-8402, Tokyo, Japan.
Yuki OgawaDepartment of Anatomy, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, 160-8402, Tokyo, Japan.
Yoshiharu MatsunoCenter for Basic Medical Research, International University of Health and Welfare, Narita Campus, 4-3 Kozunomori, Narita, 286-8686, Chiba, Japan.
Masahiro ItohDepartment of Anatomy, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, 160-8402, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cortisol/corticosterone (CORT) are typical glucocorticoids and exert an anti-stress function. p27, a cyclin-dependent kinase inhibitor, acts as a terminal factor for Sertoli cell proliferation at the prepubescent stage. Our previous study showed neonatal CORT administration increased p27-positive Sertoli cells followed by decreasing Sertoli cells in mice. The present study evaluated the effects of CORT and/or RU 486, a glucocorticoid receptor antagonist, on Sertoli cells in early life stages. CORT and/or RU 486 were subcutaneously injected to ICR mice, from postnatal days (PNDs) 1 to 10, at doses of 0.36 and 0.0006 mg/kg body weight, respectively. Testes from control, CORT-, RU 486 + CORT-, and RU 486-administered mice were evaluated on PNDs 4, 10, and 16. RU 486 administration blocked CORT-induced increase of relative p27-positive Sertoli cells, with the resultant recovery of Sertoli cell numbers to control level. RU 486 administration alone unexpectedly caused decreases in Sertoli cells. The present study is the first to reveal that activation of glucocorticoid receptors following CORT administration in early life stages is involved in p27-positive Sertoli cell and total Sertoli cell number in vivo, suggesting that appropriate glucocorticoid signaling in early life stages is required for the intact proliferation and maturation of Sertoli cells.

Indexed as

Cell ProliferationCorticosteroneMifepristoneSertoli CellsAnimalsAnimals, NewbornCyclin-Dependent Kinase Inhibitor p27MaleMiceMice, Inbred ICRReceptors, GlucocorticoidCorticosteroneCyclin-Dependent Kinase Inhibitor p27MifepristoneReceptors, GlucocorticoidCorticosteroneEarly life stressMale reproductive toxicityP27RU 486Sertoli cell number

Identifiers

PMID41436489
PMCPMC12727814

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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.