Evidence map›Paper›PMID 24838827›Full record

ArticleGlia2014

Activation of the TRPV1 cation channel contributes to stress-induced astrocyte migration.

Karen W Ho, Wendi S Lambert, David J Calkins

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, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. A 3D Astrocyte Microenvironment Model Enables Rapid CaAdvanced healthcare materials · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. TRPV1: The key bridge in neuroimmune interactions.Journal of intensive medicine · 2024
    Review
  8. Review
  9. Transient Receptor Potential Channels in the Healthy and Diseased Blood-Brain Barrier.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2024
    Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Adaptive responses to neurodegenerative stress in glaucoma.Progress in retinal and eye research · 2021
    Review
  18. Article
  19. Review
  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

3 authors at 1 institution in 1 country.

Karen W HoVanderbilt Department of Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee.
Wendi S Lambert
David J Calkins
Vanderbilt University Medical Center · US

Funding

VANDERBILT UNIVERSITY CTSA FOR PEDIATRIC RESEARCHUL1RR024975 · NCRR · VANDERBILT UNIVERSITY · PI BERNARD, GORDON RAPHAEL · 2007 to 2011
$45.7M
Shop Module CoreP30EY008126 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Kevin L Schey · 1989 to 2026
$19.6M
TRAINING IN PHARMACOLOGICAL SCIENCEST32GM007628 · NIGMS · VANDERBILT UNIVERSITY · PI BARNETT, JOEY VICTOR, KAVALALI, EGE T · 1985 to 2022
$11.2M
Transient Receptor Potential Channels and Retinal Ganglion Cell Death in GlaucomaR01EY017427 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI CALKINS, DAVID J. · 2008 to 2020
$4.2M
NCRR NIH HHS UL1 RR024975NEI NIH HHS 5R01EY017427-03NEI NIH HHS P30 EY008126NEI NIH HHS P30EY008126NEI NIH HHS R01 EY017427NIGMS NIH HHS T32 GM007628NIGMS NIH HHS T32GM007628-32
6 · The paper itself

Abstract

Astrocytes provide metabolic, structural, and synaptic support to neurons in normal physiology and also contribute widely to pathogenic processes in response to stress or injury. Reactive astrocytes can undergo cytoskeletal reorganization and increase migration through changes in intracellular Ca(2+) mediated by a variety of potential modulators. Here we tested whether migration of isolated retinal astrocytes following mechanical injury (scratch wound) involves the transient receptor potential vanilloid-1 channel (TRPV1), which contributes to Ca(2+)-mediated cytoskeletal rearrangement and migration in other systems. Application of the TRPV1-specific antagonists, capsazepine (CPZ) or 5'-iodoresiniferatoxin (IRTX), slowed migration by as much as 44%, depending on concentration. In contrast, treatment with the TRPV1-specific agonists, capsaicin (CAP) or resiniferatoxin (RTX) produced only a slight acceleration over a range of concentrations. Chelation of extracellular Ca(2+) with EGTA (1 mM) slowed astrocyte migration by 35%. Ratiometric imaging indicated that scratch wound induced a sharp 20% rise in astrocyte Ca(2+) that dissipated with distance from the wound. Treatment with IRTX both slowed and dramatically reduced the scratch-induced Ca(2+) increase. Both CPZ and IRTX influenced astrocyte cytoskeletal organization, especially near the wound edge. Taken together, our results indicate that astrocyte mobilization in response to mechanical stress involves influx of extracellular Ca(2+) and cytoskeletal changes in part mediated by TRPV1 activation.

Indexed as

Stress, MechanicalAnimalsAstrocytesCalciumCell Culture TechniquesCell MovementCells, CulturedCytoskeletonExtracellular SpaceIntracellular SpaceMice, Inbred C57BLRats, Sprague-DawleyRetinaTRPV Cation ChannelsCalciumTRPV1 protein, mouseTrpv1 protein, ratTRPV Cation ChannelsastrocytescalciummigrationreactivityTRPV1

Identifiers

PMID24838827
PMCPMC4107153
OpenAlexW1706942228

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.