Evidence map›Paper›PMID 33398046›Full record

ArticleCommunications biology2021

Age-related injury responses of human oligodendrocytes to metabolic insults: link to BCL-2 and autophagy pathways.

Milton Guilherme Forestieri Fernandes, Julia Xiao Xuan Luo, Qiao-Ling Cui, Kelly Perlman, Florian Pernin, Moein Yaqubi, Jeffery A Hall, Roy Dudley, Myriam Srour, Charles P Couturier and 6 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 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

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  16. Transcriptional and bioinformatic analysis of GABAFrontiers in molecular neuroscience · 2023
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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

16 authors at 6 institutions in 1 country.

Milton Guilherme Forestieri Fernandes *Neuroimmunology Unit, Montreal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada.ORCID http://orcid.org/0000-0002-1536-5083
Julia Xiao Xuan Luo *Neuroimmunology Unit, Montreal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada.ORCID http://orcid.org/0000-0003-2838-1231
Qiao-Ling CuiNeuroimmunology Unit, Montreal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada.
Kelly PerlmanDouglas Mental Health University Institute, 6875 Boulevard LaSalle, Verdun, QC, H4H 1R3, Canada.ORCID http://orcid.org/0000-0002-2716-0712
Florian PerninNeuroimmunology Unit, Montreal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada.
Moein YaqubiNeuroimmunology Unit, Montreal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada.
Jeffery A HallDepartment of Neurosurgery, McGill University Health Centre and Department of Neurology and Neurosurgery, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada.
Roy DudleyDepartment of Pediatric Neurosurgery, Montreal Children's Hospital, 1001 Décarie Boulevard, Montreal, QC, H4A 3J1, Canada.
Myriam SrourDivision of Pediatric Neurology, Montreal Children's Hospital, 1001 Décarie Boulevard, Montreal, QC, H4A 3J1, Canada.
Charles P CouturierDepartment of Neurosurgery, McGill University Health Centre and Department of Neurology and Neurosurgery, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada.
Kevin PetreccaDepartment of Neurosurgery, McGill University Health Centre and Department of Neurology and Neurosurgery, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada.ORCID http://orcid.org/0000-0002-8140-6402
Catherine LarochelleDepartment of Neurology, University of Montreal, 1051 Saguinet Street, Montreal, QC, H2X 3E4, Canada.
Luke M HealyNeuroimmunology Unit, Montreal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada.ORCID http://orcid.org/0000-0001-9496-2216
Jo Anne StrattonNeuroimmunology Unit, Montreal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada.
Timothy E KennedyDepartment of Neurology and Neurosurgery; Department of Human Genetics and Bioengineering, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada.
Jack P AntelNeuroimmunology Unit, Montreal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada. jack.antel@mcgill.ca.ORCID http://orcid.org/0000-0002-5148-0636
Montreal Neurological Institute and Hospital · CAMcGill University Health Centre · CAMontreal Children's Hospital · CADouglas Mental Health University Institute · CAMcGill University · CAUniversité de Montréal · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myelin destruction and oligodendrocyte (OL) death consequent to metabolic stress is a feature of CNS disorders across the age spectrum. Using cells derived from surgically resected tissue, we demonstrate that young (<age 5) pediatric-aged sample OLs are more resistant to in-vitro metabolic injury than fetal O4+ progenitor cells, but more susceptible to cell death and apoptosis than adult-derived OLs. Pediatric but not adult OLs show measurable levels of TUNEL+ cells, a feature of the fetal cell response. The ratio of anti- vs pro-apoptotic BCL-2 family genes are increased in adult vs pediatric (<age 5) mature OLs and in more mature OL lineage cells. Lysosomal gene expression was increased in adult and pediatric compared to fetal OL lineage cells. Cell death of OLs was increased by inhibiting pro-apoptotic BCL-2 gene and autophagy activity. These distinct age-related injury responses should be considered in designing therapies aimed at reducing myelin injury.

Indexed as

AutophagyStress, PhysiologicalAgingHumansOligodendrogliaPrimary Cell CultureProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-bcl-2

Identifiers

PMID33398046
PMCPMC7782481
OpenAlexW3118300061

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.