Evidence map›Paper›PMID 24740847›Full record

ArticleGlia2014

Voltage-gated sodium channel Nav 1.5 contributes to astrogliosis in an in vitro model of glial injury via reverse Na+ /Ca2+ exchange.

Laura W Pappalardo, Omar A Samad, Joel A Black, Stephen G Waxman

Abstract read
In one paragraph

Article in Glia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
–field-weighted citation impact
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

50 citing papers in PubMed.

  1. Novel NaGlia · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. NaNature · 2024
    Article
  14. Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
  15. Review
  16. Sodium regulates PLC and IPPhysiological reports · 2023
    Article
  17. USP1/UAF1-Stabilized METTL3 Promotes Reactive Astrogliosis and Improves Functional Recovery after Spinal Cord Injury through mThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  18. Activation of Glutamate Transport Increases Arteriole DiameterFrontiers in cellular neuroscience · 2022
    Article
  19. Iron induces two distinct CaCommunications biology · 2021
    Article
  20. Review
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.

Laura W PappalardoDepartment of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut; Rehabilitation Research Center, VA Connecticut Healthcare System, West Haven, Connecticut.
Omar A Samad
Joel A Black
Stephen G Waxman

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007205 · NIGMS · YALE UNIVERSITY · PI KAZMIERCZAK, BARBARA I · 1985 to 2019
$42.9M
NIGMS NIH HHS GM007205NIGMS NIH HHS T32 GM007205
6 · The paper itself

Abstract

Astrogliosis is a prominent feature of many, if not all, pathologies of the brain and spinal cord, yet a detailed understanding of the underlying molecular pathways involved in the transformation from quiescent to reactive astrocyte remains elusive. We investigated the contribution of voltage-gated sodium channels to astrogliosis in an in vitro model of mechanical injury to astrocytes. Previous studies have shown that a scratch injury to astrocytes invokes dual mechanisms of migration and proliferation in these cells. Our results demonstrate that wound closure after mechanical injury, involving both migration and proliferation, is attenuated by pharmacological treatment with tetrodotoxin (TTX) and KB-R7943, at a dose that blocks reverse mode of the Na(+) /Ca(2+) exchanger (NCX), and by knockdown of Nav 1.5 mRNA. We also show that astrocytes display a robust [Ca(2+) ]i transient after mechanical injury and demonstrate that this [Ca(2+) ]i response is also attenuated by TTX, KB-R7943, and Nav 1.5 mRNA knockdown. Our results suggest that Nav 1.5 and NCX are potential targets for modulation of astrogliosis after injury via their effect on [Ca(2+) ]i .

Indexed as

AnimalsAstrocytesCalciumCell MovementCell ProliferationCells, CulturedCerebral CortexGene Knockdown TechniquesGliosisNAV1.5 Voltage-Gated Sodium ChannelPhysical StimulationRats, Sprague-DawleyRNA, MessengerSodium-Calcium ExchangerSodium Channel BlockersTetrodotoxin2-(2-(4-(4-nitrobenzyloxy)phenyl)ethyl)isothiourea methanesulfonateCalciumNAV1.5 Voltage-Gated Sodium ChannelRNA, MessengerSodium-Calcium Exchangersodium-calcium exchanger 1Sodium Channel BlockersTetrodotoxinThioureaglial scarmigrationproliferationsodium-calcium exchangersodium channels

Identifiers

PMID24740847
PMCPMC4060891

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.