Evidence map›Paper›PMID 18191837›Full record

ArticleExperimental neurology2008

Immune activation is required for NT-3-induced axonal plasticity in chronic spinal cord injury.

Qin Chen, George M Smith, H David Shine

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

24 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. A Potential Competitive Endogenous RNA Pathway Involved in Chronic Spinal Cord Injury.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Neutrophils express oncomodulin and promote optic nerve regeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  18. Article
  19. Article
  20. Selective corticospinal tract injury in the rat induces primary afferent fiber sprouting in the spinal cord and hyperreflexia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    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 2 institutions in 1 country.

Qin ChenDepartment of Neurosurgery, Baylor College of Medicine, Houston, TX 77030, USA.
George M Smith
H David Shine
Baylor College of Medicine · USUniversity of Kentucky · US

Funding

GENE THERAPY FOR SPINAL CORD REGENERATIONR01NS038126 · NINDS · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI SMITH, GEORGE M · 1999 to 2006
$1.7M
MECHANISMS OF BRAIN TUMOR CELL DEATH AFTER GENE TRANSFERR01NS035280 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI SHINE, HAROLD DAVID · 1997 to 1999
–
NINDS NIH HHS NS 35280NINDS NIH HHS NS 38126NINDS NIH HHS R01 NS035280NINDS NIH HHS R01 NS038126
6 · The paper itself

Abstract

After an unilateral lesion of the corticospinal tract (CST) at the level of the medulla over-expression of Neurotrophin-3 (NT-3) in lumbar spinal cord motoneurons induced axonal sprouting of the intact CST in the acutely injured but not uninjured or chronically injured spinal cord in rats. This suggested that processes associated with immune-mediated wound healing may act with NT-3 to induce neuroplasticity. To test whether immune processes were involved we measured NT-3-induced axonal sprouting in immunosuppressed compared to immunocompetent rats. Rats were immunosuppressed with anti-leukocyte antibodies 1 day before receiving a CST lesion and then 2 weeks later NT-3 was over-expressed in the lumbar spinal motoneurons with an adenoviral vector carrying the NT-3 gene targeted to the motoneurons by retrograde transport. At 35 days post-lesion no axonal sprouting was measured in immunosuppressed rats whereas axonal sprouting was measured in the immunocompetent rats. We then tested whether re-evoking an immune response in chronically lesioned rats would induce neuroplasticity. Rats received CST lesions and then 4 months later were treated with systemic injections of lipopolysaccharide (LPS) 7 days before NT-3 was over-expressed in the lumbar spinal motoneurons. Axonal sprouting was observed in the LPS treated rats but not in control animals that were not treated with LPS. Further studies showed that lesioning the CST activated and LPS reactivated microglia and CD4(+) T-cells in the acutely lesioned and chronically lesioned rats, respectively. However, immunosuppression only decreased the number of activated CD4(+) T-cells suggesting they were responsible for the support of axonal growth. These observations demonstrate that processes associated with immune-mediated wound healing play a role in NT-3-induced neuroplasticity after injury.

Indexed as

Analysis of VarianceAnimalsAntigens, CDBiotinChronic DiseaseDextransDisease Models, AnimalFemaleFlow CytometryGene Expression RegulationGenetic VectorsImmunosuppressive AgentsLipopolysaccharidesMicrogliaMotor NeuronsNeuronal PlasticityAntigens, CDBiotinbiotinylated dextran amineDextransImmunosuppressive AgentsLipopolysaccharidesNeurotrophin 3

Identifiers

PMID18191837
PMCPMC2706784
OpenAlexW2053218399

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.