Evidence map›Paper›PMID 8550829›Full record

ArticleThe Journal of clinical investigation1996

Involvement of wound-associated factors in rat brain astrocyte migratory response to axonal injury: in vitro simulation.

A Faber-Elman, A Solomon, J A Abraham, M Marikovsky, M Schwartz

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.9field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 140 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Fibroblast growth factors in the management of spinal cord injury.Journal of cellular and molecular medicine · 2018
    Review
  10. Article
  11. Article
  12. Astrocytes in Migration.Neurochemical research · 2017
    Review
  13. Article
  14. In vitro models of axon regeneration.Experimental neurology · 2017
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Transforming growth factor α transforms astrocytes to a growth-supportive phenotype after spinal cord injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    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

5 authors at 2 institutions in 1 country.

A Faber-ElmanDepartment of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
A Solomon
J A Abraham
M Marikovsky
M Schwartz
Weizmann Institute of Science · ILTel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The poor ability of mammalian central nervous system (CNS) axons to regenerate has been attributed, in part, to astrocyte behavior after axonal injury. This behavior is manifested by the limited ability of astrocytes to migrate and thus repopulate the injury site. Here, the migratory behavior of astrocytes in response to injury of CNS axons in vivo was simulated in vitro using a scratch-wounded astrocytic monolayer and soluble substances derived from injured rat optic nerves. The soluble substances, applied to the scratch-wounded astrocytes, blocked their migration whereas some known wound-associated factors such as transforming growth factor-beta 1 (TGF-beta 1), basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), transforming growth factor-alpha (TGF-alpha), and heparin-binding epidermal growth factor in combination with insulin-like growth factor-1 (HB-EGF + IGF-1) stimulated intensive migration with consequent closure of the wound. Migration was not dominated by proliferating cells. Both bFGF and HB-EGF + IGF-1, but not TGF-beta 1, could overcome the blocking effect of the optic nerve-derived substances on astrocyte migration. The induced migration appeared to involve proteoglycans. It is suggestive that appropriate choice of growth factors at the appropriate postinjury period may compensate for the endogenous deficiency in glial supportive factors and/or presence of glial inhibitory factors in the CNS.

Indexed as

Nerve CrushAnimalsAstrocytesCell MovementCells, CulturedCerebral CortexChloratesChondroitin Sulfate ProteoglycansDNADrug SynergismGlial Fibrillary Acidic ProteinGrowth SubstancesHeparan SulfateHeparan Sulfate ProteoglycansHeparin LyaseNeurogliaChloratesChondroitin Sulfate ProteoglycansDNAGlial Fibrillary Acidic ProteinGrowth SubstancesHeparan SulfateHeparan Sulfate ProteoglycansHeparin LyasePolysaccharide-LyasesProteoglycanssodium chlorate

Identifiers

PMID8550829
PMCPMC507075
OpenAlexW2055867169

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.