Evidence map›Paper›PMID 39333617›Full record

ArticleScientific reports2024

Transcriptomic changes in oligodendrocyte lineage cells during the juvenile to adult transition in the mouse corpus callosum.

Tomonori Hoshino, Hajime Takase, Gen Hamanaka, Shintaro Kimura, Norito Fukuda, Emiri T Mandeville, Josephine Lok, Eng H Lo, Ken Arai

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. 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

9 authors.

Tomonori HoshinoNeuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, 149 Thirteenth Street, Room 2401, Charlestown, MA, 02129-2000, USA. thoshino@mgh.harvard.edu.
Hajime TakaseNeuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, 149 Thirteenth Street, Room 2401, Charlestown, MA, 02129-2000, USA.
Gen HamanakaNeuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, 149 Thirteenth Street, Room 2401, Charlestown, MA, 02129-2000, USA.
Shintaro KimuraNeuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, 149 Thirteenth Street, Room 2401, Charlestown, MA, 02129-2000, USA.
Norito FukudaNeuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, 149 Thirteenth Street, Room 2401, Charlestown, MA, 02129-2000, USA.
Emiri T MandevilleNeuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, 149 Thirteenth Street, Room 2401, Charlestown, MA, 02129-2000, USA.
Josephine LokNeuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, 149 Thirteenth Street, Room 2401, Charlestown, MA, 02129-2000, USA.
Eng H LoNeuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, 149 Thirteenth Street, Room 2401, Charlestown, MA, 02129-2000, USA.
Ken AraiNeuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, 149 Thirteenth Street, Room 2401, Charlestown, MA, 02129-2000, USA. karai@partners.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The corpus callosum, a major white matter tract in the brain, undergoes age-related functional changes. To extend our investigation of age-related gene expression dynamics in the mouse corpus callosum, we compared RNA-seq data from 2 week-old and 12 week-old wild-type C57BL/6 J mice and identified the differentially expressed genes (e.g., Marcksl1, Chst3, C4b, Neat1, Ndrg1, Emid1, etc.) between these ages. Interestingly, we found that genes highly expressed in myelinating oligodendrocytes were upregulated in 12 week-old mice compared to 2 week-old mice, while genes highly expressed in oligodendrocyte precursor cells (OPCs) and newly formed oligodendrocytes were downregulated. Furthermore, by comparing these genes with the datasets from 20 week-old and 96 week-old mice, we identified novel sets of genes with age-dependent variations in the corpus callosum. These gene expression changes potentially affect key biological pathways and may be closely linked to age-related neurological disorders, including dementia and stroke. Therefore, our results provide an additional dataset to explore age-dependent gene expression dynamics of oligodendrocyte lineage cells in the corpus callosum.

Indexed as

Cell LineageCorpus CallosumMice, Inbred C57BLOligodendrogliaTranscriptomeAge FactorsAgingAnimalsGene Expression ProfilingMaleMiceOligodendrocyte Precursor CellsAgingCorpus callosumDevelopmentRNA-sequencing (RNA-seq)

Identifiers

PMID39333617
PMCPMC11436962

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.