Evidence map›Paper›PMID 34127780›Full record

ArticleCommunications biology2021

A human isogenic iPSC-derived cell line panel identifies major regulators of aberrant astrocyte proliferation in Down syndrome.

Keiji Kawatani, Toshihiko Nambara, Nobutoshi Nawa, Hidetaka Yoshimatsu, Haruna Kusakabe, Katsuya Hirata, Akira Tanave, Kenta Sumiyama, Kimihiko Banno, Hidetoshi Taniguchi and 3 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Role of cystathionine-β-synthase and hydrogen sulfide in down syndrome.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  6. The RNA content of extracellular vesicles from gene-editedMolecular therapy. Methods & clinical development · 2025
    Article
  7. Article
  8. Article
  9. Isogenic iPSC-derivedFrontiers in neuroscience · 2025
    Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
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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

13 authors at 4 institutions in 1 country.

Keiji KawataniDepartment of Pediatrics, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Toshihiko NambaraDepartment of Pediatrics, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Nobutoshi NawaDepartment of Pediatrics, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.ORCID 0000-0001-6785-7867
Hidetaka YoshimatsuDepartment of Pediatrics, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Haruna KusakabeDepartment of Pediatrics, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Katsuya HirataDepartment of Pediatrics, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.ORCID 0000-0003-3148-9892
Akira TanaveLaboratory for Mouse Genetic Engineering, RIKEN Center for Biosystems Dynamics Research, Suita, Osaka, Japan.
Kenta SumiyamaLaboratory for Mouse Genetic Engineering, RIKEN Center for Biosystems Dynamics Research, Suita, Osaka, Japan.ORCID 0000-0001-8785-5439
Kimihiko BannoDepartment of Pediatrics, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Hidetoshi TaniguchiDepartment of Pediatrics, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.ORCID 0000-0002-1015-7760
Hitomi ArahoriDepartment of Pediatrics, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Keiichi OzonoDepartment of Pediatrics, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Yasuji KitabatakeDepartment of Pediatrics, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan. ykitaba@ped.med.osaka-u.ac.jp.ORCID 0000-0002-2907-9512
The University of Osaka · JPRIKEN Center for Biosystems Dynamics Research · JPNara Medical University · JPOsaka Women's and Children's Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Astrocytes exert adverse effects on the brains of individuals with Down syndrome (DS). Although a neurogenic-to-gliogenic shift in the fate-specification step has been reported, the mechanisms and key regulators underlying the accelerated proliferation of astrocyte precursor cells (APCs) in DS remain elusive. Here, we established a human isogenic cell line panel based on DS-specific induced pluripotent stem cells, the XIST-mediated transcriptional silencing system in trisomic chromosome 21, and genome/chromosome-editing technologies to eliminate phenotypic fluctuations caused by genetic variation. The transcriptional responses of genes observed upon XIST induction and/or downregulation are not uniform, and only a small subset of genes show a characteristic expression pattern, which is consistent with the proliferative phenotypes of DS APCs. Comparative analysis and experimental verification using gene modification reveal dose-dependent proliferation-promoting activity of DYRK1A and PIGP on DS APCs. Our collection of human isogenic cell lines provides a comprehensive set of cellular models for further DS investigations.

Indexed as

Cell ProliferationAstrocytesBlotting, WesternCell LineDown SyndromeGene DosageGene EditingGene SilencingHumansInduced Pluripotent Stem CellsInfant, NewbornIn Situ Hybridization, FluorescenceMale

Identifiers

PMID34127780
PMCPMC8203796
OpenAlexW3169004320

What OpenQuestion holds

Textmetadata
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.