Evidence map›Paper›PMID 31206867›Full record

ArticleBrain pathology (Zurich, Switzerland)2020

Perturbation of the immune cells and prenatal neurogenesis by the triplication of the Erg gene in mouse models of Down syndrome.

Keiichi Ishihara, Ryohei Shimizu, Kazuyuki Takata, Eri Kawashita, Kenji Amano, Atsushi Shimohata, Donovan Low, Takeshi Nabe, Haruhiko Sago, Warren S Alexander and 3 more

Abstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
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  6. Review
  7. Down syndrome: A curative prospect?AIMS neuroscience · 2020
    Review
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.

Keiichi IshiharaDepartment of Pathological Biochemistry, Division of Pathological Sciences, Kyoto Pharmaceutical University, Kyoto, Japan.ORCID 0000-0001-8748-7218
Ryohei ShimizuDepartment of Pathological Biochemistry, Division of Pathological Sciences, Kyoto Pharmaceutical University, Kyoto, Japan.
Kazuyuki TakataDepartment of Clinical and Translational Physiology, Division of Biological Sciences, Kyoto Pharmaceutical University, Kyoto, Japan.
Eri KawashitaDepartment of Pathological Biochemistry, Division of Pathological Sciences, Kyoto Pharmaceutical University, Kyoto, Japan.
Kenji AmanoLaboratory for Neurogenetics, RIKEN Center for Brain Science, Saitama, Japan.
Atsushi ShimohataLaboratory for Neurogenetics, RIKEN Center for Brain Science, Saitama, Japan.
Donovan LowSingapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
Takeshi NabeLaboratory of Immunopharmacology, Faculty of Pharmaceutical Sciences, Setsunan University, Osaka, Japan.
Haruhiko SagoCenter for Maternal-Fetal, Neonatal and Reproductive Medicine, National Center for Child Health and Development, Tokyo, Japan.
Warren S AlexanderCancer and Haematology Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia.
Florent GinhouxSingapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
Kazuhiro YamakawaLaboratory for Neurogenetics, RIKEN Center for Brain Science, Saitama, Japan.
Satoshi AkibaDepartment of Pathological Biochemistry, Division of Pathological Sciences, Kyoto Pharmaceutical University, Kyoto, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Some mouse models of Down syndrome (DS), including Ts1Cje mice, exhibit impaired prenatal neurogenesis with yet unknown molecular mechanism. To gain insights into the impaired neurogenesis, a transcriptomic and flow cytometry analysis of E14.5 Ts1Cje embryo brain was performed. Our analysis revealed that the neutrophil and monocyte ratios in the CD45-positive hematopoietic cells were relatively increased, in agreement with the altered expression of inflammation/immune-related genes, in Ts1Cje embryonic brain, whereas the relative number of brain macrophages was decreased in comparison to wild-type mice. Similar upregulation of inflammation-associated mRNAs was observed in other DS mouse models, with variable trisomic region lengths. We used genetic manipulation to assess the contribution of Erg, a trisomic gene in these DS models, known to regulation hemato-immune cells. The perturbed proportions of immune cells in Ts1Cje mouse brain were restored in Ts1Cje-Erg

Indexed as

AnimalsBrainDisease Models, AnimalDown SyndromeFemaleHumansMiceMice, Inbred C57BLMice, TransgenicNeurogenesisOncogene ProteinsPregnancyTranscriptional Regulator ERGTranscriptomeERG protein, humanERG protein, mouseOncogene ProteinsTranscriptional Regulator ERGDown syndromeimmune cellsmouse modelsprenatal neurogenesistranscriptional factor Ergtranscriptomics

Identifiers

PMID31206867
PMCPMC8018000

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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.