Evidence map›Paper›PMID 10493720›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

Cellular and molecular mechanisms of glial scarring and progressive cavitation: in vivo and in vitro analysis of inflammation-induced secondary injury after CNS trauma.

M T Fitch, C Doller, C K Combs, G E Landreth, J Silver

Open access · greenAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 203 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
203citing papers in PubMed, 1 pooled it
11.3field-weighted citation impact, top 1% 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

203 citing papers in PubMed, 1 synthesis or guideline pooled it, 558 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Regeneration in fish, with special focus on killifishes.Fish physiology and biochemistry · 2025
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Frontiers in bioengineering and biotechnology · 2024
    Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

143 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

5 authors at 1 institution in 1 country.

M T FitchDepartment of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA.
C Doller
C K Combs
G E Landreth
J Silver
University School · US

Funding

FACTORS AFFECTING REGENERATION THRU THE GLIAL SCARR01NS025713 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI SILVER, JERRY · 1988 to 2016
$3.1M
Factors Affecting Regeneration Through the Glial ScarR37NS025713 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI SILVER, JERRY · 2005 to 2011
$2.7M
NINDS NIH HHS NS25713
6 · The paper itself

Abstract

Post-traumatic cystic cavitation, in which the size and severity of a CNS injury progress from a small area of direct trauma to a greatly enlarged secondary injury surrounded by glial scar tissue, is a poorly understood complication of damage to the brain and spinal cord. Using minimally invasive techniques to avoid primary physical injury, this study demonstrates in vivo that inflammatory processes alone initiate a cascade of secondary tissue damage, progressive cavitation, and glial scarring in the CNS. An in vitro model allowed us to test the hypothesis that specific molecules that stimulate macrophage inflammatory activation are an important step in initiating secondary neuropathology. Time-lapse video analyses of inflammation-induced cavitation in our in vitro model revealed that this process occurs primarily via a previously undescribed cellular mechanism involving dramatic astrocyte morphological changes and rapid migration. The physical process of cavitation leads to astrocyte abandonment of neuronal processes, neurite stretching, and secondary injury. The macrophage mannose receptor and the complement receptor type 3 beta2-integrin are implicated in the cascade that induces cavity and scar formation. We also demonstrate that anti-inflammatory agents modulating transcription via the nuclear hormone receptor peroxisome proliferator-activated receptor-gamma may be therapeutic in preventing progressive cavitation by limiting inflammation and subsequent secondary damage after CNS injury.

Indexed as

InflammationThiazolidinedionesAnimalsAnimals, NewbornAstrocytesAxonsBrain InjuriesCell MovementCells, CulturedCerebral CortexGanglia, SpinalGene Expression RegulationGlial Fibrillary Acidic ProteinIndomethacinLipopolysaccharidesMacrophage ActivationciglitazoneGlial Fibrillary Acidic ProteinIndomethacinLipopolysaccharidesProteoglycansThiazolesThiazolidinedionesZymosan

Identifiers

PMID10493720
PMCPMC6783021
OpenAlexW2115352319

What OpenQuestion holds

Textmetadata
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.