Evidence map›Paper›PMID 25542980›Full record

ArticleExperimental neurology2015

Voltage-gated Ca2+ entry promotes oligodendrocyte progenitor cell maturation and myelination in vitro.

V T Cheli, D A Santiago González, V Spreuer, P M Paez

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

67 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Transferrin Receptor Is Necessary for Proper Oligodendrocyte Iron Homeostasis and Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  17. Blockade of L-Type CaCurrent issues in molecular biology · 2023
    Article
  18. Article
  19. Article
  20. Article

7 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

V T CheliHunter James Kelly Research Institute, Department of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, SUNY, University at Buffalo, NYS Center of Excellence, 701 Ellicott St., Buffalo, NY 14203, USA.
D A Santiago GonzálezHunter James Kelly Research Institute, Department of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, SUNY, University at Buffalo, NYS Center of Excellence, 701 Ellicott St., Buffalo, NY 14203, USA.
V SpreuerHunter James Kelly Research Institute, Department of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, SUNY, University at Buffalo, NYS Center of Excellence, 701 Ellicott St., Buffalo, NY 14203, USA.
P M PaezHunter James Kelly Research Institute, Department of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, SUNY, University at Buffalo, NYS Center of Excellence, 701 Ellicott St., Buffalo, NY 14203, USA. Electronic address: ppaez@buffalo.edu.
University at Buffalo, State University of New York · US

Funding

Protein Targets of Oxidative Brain AgingP01AG022550 · NIA · WEST VIRGINIA UNIVERSITY · PI SIMPKINS, JAMES W. · 2003 to 2013
$15.7M
System Gene Delivery for Alzheimer's Disease- SupplementP01AG010485 · NIA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI ZOLOTUKHIN, SERGEI · 1991 to 2009
$11.3M
ROLE OF MITHOCHONDRIAL ERB IN NEURONAL VULNDERABILITY TO NEUROTOXIC STRESSP01AG027956 · NIA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI SINGH, MEHARVAN · 2007 to 2017
$11.3M
Modulation of Oligodendrocyte Development by Voltage-Operated Calcium ChannelsR01NS078041 · NINDS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI Pablo Martin Paez · 2013 to 2026
$3.8M
Mechanisms of calcium signaling in retinal neuronsR01EY014227 · NEI · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI KOULEN, PETER · 2003 to 2006
$1.6M
Novel mechanism of action as therapeutic strategy for optic neuritisR01EY022774 · NEI · UNIVERSITY OF MISSOURI KANSAS CITY · PI KOULEN, PETER · 2012 to 2014
$1.2M
Confocal Laser Scanning MicroscopeS10RR027093 · NCRR · UNIVERSITY OF MISSOURI KANSAS CITY · PI KOULEN, PETER · 2010 to 2010
$497k
CONFOCAL MICROSCOPE FOR CAMPUS EXPANSION IN THE CBH BUILDING: NEUROSCIENCES10RR022570 · NCRR · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI KOULEN, PETER · 2006 to 2006
$356k
NCRR NIH HHS RR022570NCRR NIH HHS RR027093NEI NIH HHS EY014227NEI NIH HHS EY022774NIA NIH HHS AG010485NIA NIH HHS AG022550NIA NIH HHS AG027956NINDS NIH HHS R01 NS078041
6 · The paper itself

Abstract

We have previously shown that the expression of voltage-operated Ca(++) channels (VOCCs) is highly regulated in the oligodendroglial lineage and is essential for proper oligodendrocyte progenitor cell (OPC) migration. Here we assessed the role of VOCCs, in particular the L-type, in oligodendrocyte maturation. We used pharmacological treatments to activate or block voltage-gated Ca(++) uptake and siRNAs to specifically knock down the L-type VOCC in primary cultures of mouse OPCs. Activation of VOCCs by plasma membrane depolarization increased OPC morphological differentiation as well as the expression of mature oligodendrocyte markers. On the contrary, inhibition of L-type Ca(++) channels significantly delayed OPC development. OPCs transfected with siRNAs for the Cav1.2 subunit that conducts L-type Ca(++) currents showed reduce Ca(++) influx by ~75% after plasma membrane depolarization, indicating that Cav1.2 is heavily involved in mediating voltage-operated Ca(++) entry in OPCs. Cav1.2 knockdown induced a decrease in the proportion of oligodendrocytes that expressed myelin proteins, and an increase in cells that retained immature oligodendrocyte markers. Moreover, OPC proliferation, but not cell viability, was negatively affected after L-type Ca(++) channel knockdown. Additionally, we have tested the ability of L-type VOCCs to facilitate axon-glial interaction during the first steps of myelin formation using an in vitro co-culture system of OPCs with cortical neurons. Unlike control OPCs, Cav1.2 deficient oligodendrocytes displayed a simple morphology, low levels of myelin proteins expression and appeared to be less capable of establishing contacts with neurites and axons. Together, this set of in vitro experiments characterizes the involvement of L-type VOCCs on OPC maturation as well as the role played by these Ca(++) channels during the early phases of myelination.

Indexed as

AnimalsAnimals, NewbornBase SequenceCalcium Channels, L-TypeCell DifferentiationCells, CulturedCerebral CortexCoculture TechniquesGene Knockdown TechniquesMiceMolecular Sequence DataMyelin SheathNeurogenesisOligodendrogliaStem CellsCACNA1C protein, mouseCacna1d protein, mouseCalcium Channels, L-TypeCalcium influxMyelinationOligodendrocyteVoltage-operated Ca(++) channels

Identifiers

PMID25542980
PMCPMC4711374
OpenAlexW2074926091

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.