Evidence map›Paper›PMID 19224580›Full record

ArticleJournal of neuroscience research2009

Adult CST-null mice maintain an increased number of oligodendrocytes.

S M Shroff, A D Pomicter, W N Chow, M A Fox, R J Colello, S C Henderson, J L Dupree

Abstract read
In one paragraph

Article in Journal of neuroscience research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  7. Review
  8. Review
  9. Defining Changes in the Spatial Distribution and Composition of Brain Lipids in the Shiverer and Cuprizone Mouse Models of Myelin Disease.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019
    Article
  10. Article
  11. Article
  12. Review
  13. Defects of Lipid Synthesis Are Linked to the Age-Dependent Demyelination Caused by Lamin B1 Overexpression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  14. Article
  15. Biosynthesis and biological function of sulfoglycolipids.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2013
    Review
  16. Article
  17. Review
  18. Article
  19. Increased numbers of oligodendrocyte lineage cells in the optic nerves of cerebroside sulfotransferase knockout mice.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2011
    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

7 authors at 1 institution in 1 country.

S M ShroffDepartment of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, USA.
A D Pomicter
W N Chow
M A Fox
R J Colello
S C Henderson
J L Dupree
Virginia Commonwealth University · US

Funding

VCU Neuroscience Center Core GrantP30NS047463 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI POVLISHOCK, JOHN T · 2003 to 2013
$5.0M
Generation of a floxed CST mouseR03NS071303 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI DUPREE, JEFFREY L. · 2010 to 2011
$148k
NINDS NIH HHS P30 NS047463NINDS NIH HHS R03 NS071303
6 · The paper itself

Abstract

The galactolipids galactocerebroside and sulfatide have been implicated in oligodendrocyte (OL) development and myelin formation. Much of the early evidence for myelin galactolipid function has been derived from antibody and chemical perturbation of OLs in vitro. To determine the role of these lipids in vivo, we previously characterized mice lacking galactocerebroside and sulfatide and observed abundant, unstable myelin and an increased number of OLs. We have also reported that mice incapable of synthesizing sulfatide (CST-null) while maintaining normal levels of galactocerebroside generate relatively stable myelin with unstable paranodes. Additionally, Hirahara et al. (2004; Glia 45:269-277) reported that these CST-null mice also contain an increased number of OLs in the forebrain, medulla, and cerebellum at 7 days of age. Here, we further the findings of Hirahara et al. by demonstrating that the number of OLs in the CST-null mice is also increased in the spinal cord and that this elevated OL population is maintained through, at least, 7 months of age. Moreover, we show that the enhanced OL population is accompanied by increased proliferation and decreased apoptosis of oligodendrocytic-lineage cells. Finally, through ultrastructural analysis, we show that the CST-null OLs exhibit decreased morphological complexity, a feature that may result in decreased OL competition and increased OL survival.

Indexed as

Cell ProliferationAgingAnimalsApoptosisCell CountCell DifferentiationCell LineageCell SurvivalDisease Models, AnimalGene Expression RegulationHereditary Central Nervous System Demyelinating DiseasesMiceMice, KnockoutMyelin SheathNerve Fibers, MyelinatedOligodendrogliagalactosylceramide sulfotransferaseSulfoglycosphingolipidsSulfotransferases

Identifiers

PMID19224580
PMCPMC4964850
OpenAlexW2068198420

What OpenQuestion holds

Textmetadata
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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.