Evidence map›Paper›PMID 34010640›Full record

ArticleCell reports2021

GluA2 overexpression in oligodendrocyte progenitors promotes postinjury oligodendrocyte regeneration.

Rabia R Khawaja, Amit Agarwal, Masahiro Fukaya, Hey-Kyeong Jeong, Scott Gross, Estibaliz Gonzalez-Fernandez, Jonathan Soboloff, Dwight E Bergles, Shin H Kang

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.8field-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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  5. Review
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  7. Review
  8. The Many Lives of an Oligodendrocyte Precursor Cell.Annual review of neuroscience · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Features, Fates, and Functions of Oligodendrocyte Precursor Cells.Cold Spring Harbor perspectives in biology · 2024
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. A comparative analysis of microglial inducible Cre lines.bioRxiv : the preprint server for biology · 2023
    Article
  20. 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 at 4 institutions in 3 countries.

Rabia R KhawajaCenter for Neural Repair and Rehabilitation (Shriners Hospitals of Pediatric Research Center), Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA; Department of Anatomy and Cell Biology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Amit AgarwalThe Solomon Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21025, USA; The Chica and Heinz Schaller Research Group, Institute for Anatomy and Cell Biology, Heidelberg University, 69120 Heidelberg, Germany; Interdisciplinary Center for Neurosciences, Heidelberg University, 69120 Heidelberg, Germany.
Masahiro FukayaDepartment of Anatomy, Kitasato University School of Medicine, Sagamihara, Kanagawa 252-0374, Japan.
Hey-Kyeong JeongCenter for Neural Repair and Rehabilitation (Shriners Hospitals of Pediatric Research Center), Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Scott GrossFels Cancer Institute for Personalized Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Estibaliz Gonzalez-FernandezCenter for Neural Repair and Rehabilitation (Shriners Hospitals of Pediatric Research Center), Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Jonathan SoboloffFels Cancer Institute for Personalized Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Dwight E BerglesThe Solomon Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21025, USA; Kavli Neuroscience Discovery Institute, Johns Hopkins University, Baltimore, MD 21205, USA.
Shin H KangCenter for Neural Repair and Rehabilitation (Shriners Hospitals of Pediatric Research Center), Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA; Department of Anatomy and Cell Biology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA. Electronic address: shin.kang@temple.edu.
Temple University Hospital · USJohns Hopkins University · USTemple University · USKitasato University · JP

Funding

Bronx-Einstein Training in Teaching and Research (BETTR), an IRACDA programK12GM102779 · NIGMS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI Dianne Cox, Johanna Patricia Daily · 2012 to 2026
$9.2M
Role of Oligodendroglia in the Pathogenesis of ALSR01NS089586 · NINDS · TEMPLE UNIV OF THE COMMONWEALTH · PI KANG, SHIN H · 2016 to 2020
$2.1M
Defining STIM1 function at the Immunological SynapseR01AI152506 · NIAID · TEMPLE UNIV OF THE COMMONWEALTH · PI SOBOLOFF, JONATHAN A · 2020 to 2024
$2.0M
EGR-mediated STIM1-PMCA expression and function in T cell subsetsR01GM117907 · NIGMS · TEMPLE UNIV OF THE COMMONWEALTH · PI SOBOLOFF, JONATHAN A · 2016 to 2019
$1.6M
Role of NG2+ glial cells in recovery from spinal cord injuryR21NS092009 · NINDS · JOHNS HOPKINS UNIVERSITY · PI BELEGU, VISAR, BERGLES, DWIGHT E · 2015 to 2016
$446k
NIAID NIH HHS R01 AI152506NIGMS NIH HHS K12 GM102779NIGMS NIH HHS R01 GM117907NINDS NIH HHS R01 NS089586NINDS NIH HHS R21 NS092009
6 · The paper itself

Abstract

Oligodendrocyte precursor cells (OPCs) are essential for developmental myelination and oligodendrocyte regeneration after CNS injury. These progenitors express calcium-permeable AMPA receptors (AMPARs) and form direct synapses with neurons throughout the CNS, but the roles of this signaling are unclear. To enable selective alteration of the properties of AMPARs in oligodendroglia, we generate mice that allow cell-specific overexpression of EGFP-GluA2 in vivo. In healthy conditions, OPC-specific GluA2 overexpression significantly increase their proliferation in an age-dependent manner but did not alter their rate of differentiation into oligodendrocytes. In contrast, after demyelinating brain injury in neonates or adults, higher GluA2 levels promote both OPC proliferation and oligodendrocyte regeneration, but do not prevent injury-induced initial cell loss. These findings indicate that AMPAR GluA2 content regulates the proliferative and regenerative behavior of adult OPCs, serving as a putative target for better myelin repair.

Indexed as

AnimalsCell ProliferationMiceOligodendrocyte Precursor CellsOligodendrogliaRatsReceptors, AMPARegenerationglutamate receptor ionotropic, AMPA 2Receptors, AMPAAMPA receptorcalciumGluA2hypoxic-ischemiainjuryoligodendrocyteOPCremyelination

Identifiers

PMID34010640
PMCPMC8185898
OpenAlexW3160106214

What OpenQuestion 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 OpenQuestion graph.