Evidence map›Paper›PMID 36897562›Full record

ArticleDevelopment (Cambridge, England)2023

Glutamine protects mouse spermatogonial stem cells against NOX1-derived ROS for sustaining self-renewal division in vitro.

Takehiro Miyazaki, Mito Kanatsu-Shinohara, Narumi Ogonuki, Shogo Matoba, Atsuo Ogura, Chihiro Yabe-Nishimura, Hongliang Zhang, Yves Pommier, Andreas Trumpp, Takashi Shinohara

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.8field-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

9 citing papers in PubMed, 14 citations in OpenAlex.

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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

10 authors at 5 institutions in 3 countries.

Takehiro MiyazakiDepartment of Molecular Genetics, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.
Mito Kanatsu-ShinoharaDepartment of Molecular Genetics, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.ORCID 0000-0002-9613-7022
Narumi OgonukiRIKEN, Bioresource Research Center, Tsukuba 305-0074, Japan.
Shogo MatobaRIKEN, Bioresource Research Center, Tsukuba 305-0074, Japan.
Atsuo OguraRIKEN, Bioresource Research Center, Tsukuba 305-0074, Japan.
Chihiro Yabe-NishimuraDeparment of Pharmacology, Kyoto Prefectural University of Medicine, Kyoto 606-8566, Japan.
Hongliang ZhangDeveopmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institute of Health, Bethesda, MD 20892, USA.
Yves PommierDeveopmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institute of Health, Bethesda, MD 20892, USA.
Andreas TrumppDivision of Stem Cells and Cancer, Deutsches Krebsforshungszentrum (DKFZ), 69120 Heidelberg, Germany.ORCID 0000-0002-6212-3466
Takashi ShinoharaDepartment of Molecular Genetics, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.
Kyoto University · JPRIKEN BioResource Research Center · JPNational Cancer Institute · USHeidelberg University · DEKyoto Prefectural University of Medicine · JP

Funding

DNA Repair, Cell Cycle Checkpoints and Apoptosis as Targets for Anticancer DrugsZIABC006150 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POMMIER, YVES · 2009 to 2025
$23.0M
Ministry of Education, Culture, Sports, Science and Technology 22K19429
6 · The paper itself

Abstract

Reactive oxygen species (ROS) are generated from NADPH oxidases and mitochondria; they are generally harmful for stem cells. Spermatogonial stem cells (SSCs) are unique among tissue-stem cells because they undergo ROS-dependent self-renewal via NOX1 activation. However, the mechanism by which SSCs are protected from ROS remains unknown. Here, we demonstrate a crucial role for Gln in ROS protection using cultured SSCs derived from immature testes. Measurements of amino acids required for SSC cultures revealed the indispensable role of Gln in SSC survival. Gln induced Myc expression to drive SSC self-renewal in vitro, whereas Gln deprivation triggered Trp53-dependent apoptosis and impaired SSC activity. However, apoptosis was attenuated in cultured SSCs that lacked NOX1. In contrast, cultured SSCs lacking Top1mt mitochondria-specific topoisomerase exhibited poor mitochondrial ROS production and underwent apoptosis. Gln deprivation reduced glutathione production; supra-molar Asn supplementation allowed offspring production from SSCs cultured without Gln. Therefore, Gln ensures ROS-dependent SSC-self-renewal by providing protection against NOX1 and inducing Myc.

Indexed as

GlutamineSpermatogoniaAnimalsCell ProliferationCells, CulturedMaleMiceReactive Oxygen SpeciesStem CellsGlutamineReactive Oxygen SpeciesGlutamineNox1Reactive oxygen speciesSpermatogonial stem cells

Identifiers

PMID36897562
PMCPMC10698750
OpenAlexW4323806093

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.