Evidence map›Paper›PMID 22437915›Full record

ArticleJournal of neuroscience research2012

Myosin II is a negative regulator of oligodendrocyte morphological differentiation.

Haibo Wang, Tomasz Rusielewicz, Ambika Tewari, Ellen M Leitman, Steven Einheber, Carmen V Melendez-Vasquez

Open access · greenAbstract read
In one paragraph

Article in Journal of neuroscience research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

32 citing papers in PubMed, 45 citations in OpenAlex.

  1. HMolecular neurobiology · 2023
    Review
  2. Myelination dictates axonal viscoelasticity.The European journal of neuroscience · 2023
    Article
  3. Article
  4. Group I PAKs in myelin formation and repair of the central nervous system: what, when, and how.Biological reviews of the Cambridge Philosophical Society · 2022
    Review
  5. Functional Role of Non-Muscle Myosin II in Microglia: An Updated Review.International journal of molecular sciences · 2021
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

6 authors at 2 institutions in 1 country.

Haibo WangDepartment of Biological Sciences, Hunter College, City University of New York, New York, New York 10065, USA.
Tomasz Rusielewicz
Ambika Tewari
Ellen M Leitman
Steven Einheber
Carmen V Melendez-Vasquez
City University of New York · USHunter College · US

Funding

WILD TYPE &MUTANT P53 INTERACTIONS WITH HIV LTR DNAG12RR003037 · NCRR · HUNTER COLLEGE · PI DOTTIN, ROBERT P · 1985 to 2011
$27.6M
Basic and Translational Research Center for Reducing Health DisparitiesG12MD007599 · NIMHD · HUNTER COLLEGE · PI ANGULO, JESUS A · 2012 to 2017
$14.6M
Actomyosin motors and Mechanism of Myelin FormationR01NS052259 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI MELENDEZ-VASQUEZ, CARMEN V · 2005 to 2010
$1.7M
Regulation of myelination by myosin II-mediated mechanotransductionSC1NS000001 · NINDS · HUNTER COLLEGE · PI MELENDEZ-VASQUEZ, CARMEN V · 2013 to 2016
$1.4M
Howard Hughes Medical InstituteNCRR NIH HHS G12 RR003037NCRR NIH HHS RR03037NIMHD NIH HHS G12 MD007599NINDS NIH HHS NS052259NINDS NIH HHS R01 NS052259NINDS NIH HHS SC1 NS000001
6 · The paper itself

Abstract

During their development as myelinating cells, oligodendrocyte progenitors (OPC) undergo dramatic changes in the organization of their cytoskeleton. These changes involve an increase in cell branching and in lamella extension, which is important for the ability of oligodendrocytes to myelinate multiple axons in the CNS. We have previously shown that the levels of the actin-associated motor protein nonmuscle myosin II (NMII) decrease as oligodendrocyte differentiate and that inhibition of NMII activity increases branching and myelination, suggesting that NMII is a negative regulator of oligodendrocyte differentiation. In agreement with this interpretation, we have found that overexpression of NMII prevents oligodendrocyte branching and differentiation and that OPC maturation is accelerated in NMII knockout mice as shown by a significant increase in the percentage of mature MBP(+) cells. Although several pathways have been implicated in oligodendrocyte morphogenesis, their specific contribution to the regulation of NMII activity has not been directly examined. We tested the hypothesis that the activity of NMII in OPC is controlled by Fyn kinase via downregulation of RhoA-ROCK-NMII phosphorylation. We found that treatment with PP2 or knockdown of Fyn using siRNA prevents the decrease in myosin phosphorylation normally observed during OPC differentiation and that the inhibition of branching induced by overexpression of constitutively active RhoA can be reversed by treatment with Y27632 or blebbistatin. Taken together, our results demonstrate that Fyn kinase downregulates NMII activity, thus promoting oligodendrocyte morphological differentiation.

Indexed as

AnimalsCell DifferentiationCytoskeletonDown-RegulationFluorescent Antibody TechniqueMiceMice, KnockoutMicroscopy, ImmunoelectronMyosin Type IINeural Stem CellsNeurogenesisOligodendrogliaPhosphorylationProto-Oncogene Proteins c-fynRatsSignal TransductionMyosin Type IIProto-Oncogene Proteins c-fyn

Identifiers

PMID22437915
PMCPMC3370114
OpenAlexW1991155053

What OpenQuestion holds

Textmetadata
LicenceTDM
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.