Evidence map›Paper›PMID 33942723›Full record

ArticleeLife2021

Co-targeting myelin inhibitors and CSPGs markedly enhances regeneration of GDNF-stimulated, but not conditioning-lesioned, sensory axons into the spinal cord.

Jinbin Zhai, Hyukmin Kim, Seung Baek Han, Meredith Manire, Rachel Yoo, Shuhuan Pang, George M Smith, Young-Jin Son

Open access · goldAbstract read
In one paragraph

Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Cytokine Signalling at the Microglial Penta-Partite Synapse.International journal of molecular sciences · 2021
    Review
  6. Review
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

8 authors at 1 institution in 1 country.

Jinbin ZhaiShriners Hospitals Pediatric Research Center and Center for Neural Repair and Rehabilitation, Lewis Katz School of Medicine, Temple University, Philadelphia, United States.
Hyukmin KimShriners Hospitals Pediatric Research Center and Center for Neural Repair and Rehabilitation, Lewis Katz School of Medicine, Temple University, Philadelphia, United States.
Seung Baek HanShriners Hospitals Pediatric Research Center and Center for Neural Repair and Rehabilitation, Lewis Katz School of Medicine, Temple University, Philadelphia, United States.
Meredith ManireShriners Hospitals Pediatric Research Center and Center for Neural Repair and Rehabilitation, Lewis Katz School of Medicine, Temple University, Philadelphia, United States.
Rachel YooShriners Hospitals Pediatric Research Center and Center for Neural Repair and Rehabilitation, Lewis Katz School of Medicine, Temple University, Philadelphia, United States.
Shuhuan PangShriners Hospitals Pediatric Research Center and Center for Neural Repair and Rehabilitation, Lewis Katz School of Medicine, Temple University, Philadelphia, United States.
George M SmithShriners Hospitals Pediatric Research Center and Center for Neural Repair and Rehabilitation, Lewis Katz School of Medicine, Temple University, Philadelphia, United States.
Young-Jin SonShriners Hospitals Pediatric Research Center and Center for Neural Repair and Rehabilitation, Lewis Katz School of Medicine, Temple University, Philadelphia, United States.ORCID 0000-0001-5725-9775
Temple University · US

Funding

Dorsal root injury and repairR01NS079631 · NINDS · TEMPLE UNIV OF THE COMMONWEALTH · PI SON, YOUNG-JIN · 2013 to 2017
$1.7M
NINDS NIH HHS R01 NS079631
6 · The paper itself

Abstract

A major barrier to intraspinal regeneration after dorsal root (DR) injury is the DR entry zone (DREZ), the CNS/PNS interface. DR axons stop regenerating at the DREZ, even if regenerative capacity is increased by a nerve conditioning lesion. This potent blockade has long been attributed to myelin-associated inhibitors and (CSPGs), but incomplete lesions and conflicting reports have prevented conclusive agreement. Here, we evaluated DR regeneration in mice using novel strategies to facilitate complete lesions and analyses, selective tracing of proprioceptive and mechanoreceptive axons, and the first simultaneous targeting of Nogo/Reticulon-4, MAG, OMgp, CSPGs, and GDNF. Co-eliminating myelin inhibitors and CSPGs elicited regeneration of only a few conditioning-lesioned DR axons across the DREZ. Their absence, however, markedly and synergistically enhanced regeneration of GDNF-stimulated axons, highlighting the importance of sufficiently elevating intrinsic growth capacity. We also conclude that myelin inhibitors and CSPGs are not the primary mechanism stopping axons at the DREZ.

Indexed as

AnimalsAxonsFemaleGlial Cell Line-Derived Neurotrophic FactorMaleMiceMice, Inbred C57BLMice, KnockoutMyelin SheathSpinal CordSpinal Nerve RootsGlial Cell Line-Derived Neurotrophic Factordorsal root injuryDRGmouseneuroscienceNogorhizotomysensory axonspinal cord regeneration

Identifiers

PMID33942723
PMCPMC8139830
OpenAlexW3158527779

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.