Evidence map›Paper›PMID 24168314›Full record

ArticleTissue engineering. Part A2014

Long-term characterization of axon regeneration and matrix changes using multiple channel bridges for spinal cord regeneration.

Hannah M Tuinstra, Daniel J Margul, Ashley G Goodman, Ryan M Boehler, Samantha J Holland, Marina L Zelivyanskaya, Brian J Cummings, Aileen J Anderson, Lonnie D Shea

Abstract read
In one paragraph

Article in Tissue engineering. Part A, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
–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

25 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Nanoparticle and epothilone D combinatorial intervention improves motor performance and regeneration in chronic cervical spinal cord injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Regenerative Therapies for Spinal Cord Injury.Tissue engineering. Part B, Reviews · 2019
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  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

9 authors.

Hannah M Tuinstra1 Department of Chemical and Biological Engineering, Northwestern University , Evanston, Illinois.
Daniel J Margul
Ashley G Goodman
Ryan M Boehler
Samantha J Holland
Marina L Zelivyanskaya
Brian J Cummings
Aileen J Anderson
Lonnie D Shea

Funding

Regenerative Scaffold Technologies for CNS and DiabetesR01EB003806 · NIBIB · NORTHWESTERN UNIVERSITY AT CHICAGO · PI STUPP, SAMUEL I · 2004 to 2015
$10.7M
Controlled Release Scaffolds for Nerve RegenerationR01EB005678 · NIBIB · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ANDERSON, AILEEN J, SHEA, LONNIE D · 2007 to 2018
$6.0M
Parallel gene delivery from spinal cord bridgesR21EB006520 · NIBIB · NORTHWESTERN UNIVERSITY · PI SHEA, LONNIE D · 2007 to 2008
$383k
NIBIB NIH HHS R01 EB003806NIBIB NIH HHS R01 EB005678NIBIB NIH HHS R21 EB006520
6 · The paper itself

Abstract

Spinal cord injury (SCI) results in loss of sensory and motor function below the level of injury and has limited available therapies. The host response to SCI is typified by limited endogenous repair, and biomaterial bridges offer the potential to alter the microenvironment to promote regeneration. Porous multiple channel bridges implanted into the injury provide stability to limit secondary damage and support cell infiltration that limits cavity formation. At the same time, the channels provide a path that physically directs axon growth across the injury. Using a rat spinal cord hemisection injury model, we investigated the dynamics of axon growth, myelination, and scar formation within and around the bridge in vivo for 6 months, at which time the bridge has fully degraded. Axons grew into and through the channels, and the density increased overtime, resulting in the greatest axon density at 6 months postimplantation, despite complete degradation of the bridge by that time point. Furthermore, the persistence of these axons contrasts with reports of axonal dieback in other models and is consistent with axon stability resulting from some degree of connectivity. Immunostaining of axons revealed both motor and sensory origins of the axons found in the channels of the bridge. Extensive myelination was observed throughout the bridge at 6 months, with centrally located and peripheral channels seemingly myelinated by oligodendrocytes and Schwann cells, respectively. Chondroitin sulfate proteoglycan deposition was restricted to the edges of the bridge, was greatest at 1 week, and significantly decreased by 6 weeks. The dynamics of collagen I and IV, laminin, and fibronectin deposition varied with time. These studies demonstrate that the bridge structure can support substantial long-term axon growth and myelination with limited scar formation.

Indexed as

Spinal Cord RegenerationAcetylcholinesteraseAnimalsAxonsCalcitonin Gene-Related PeptideChondroitin SulfatesCollagen Type ICollagen Type IVExtracellular MatrixFemaleFibronectinsLamininMyelin SheathRatsRats, Long-EvansSpinal Cord InjuriesAcetylcholinesteraseCalcitonin Gene-Related PeptideChondroitin SulfatesCollagen Type ICollagen Type IVFibronectinsLaminin

Identifiers

PMID24168314
PMCPMC3938917

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.