Evidence map›Paper›PMID 25698749›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015

Overexpression of Sox11 promotes corticospinal tract regeneration after spinal injury while interfering with functional recovery.

Zimei Wang, Ashley Reynolds, Adam Kirry, Christopher Nienhaus, Murray G Blackmore

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

104 citing papers in PubMed, 165 citations in OpenAlex.

  1. Article
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  4. CircadianZoological research · 2026
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  18. Lipin1 depletion coordinates neuronal signaling pathways to promote motor and sensory axon regeneration after spinal cord injury.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  19. Article
  20. Article

44 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.

Zimei WangDepartment of Biomedical Sciences, Marquette University, Milwaukee, Wisconsin 53201.
Ashley ReynoldsDepartment of Biomedical Sciences, Marquette University, Milwaukee, Wisconsin 53201.
Adam KirryDepartment of Biomedical Sciences, Marquette University, Milwaukee, Wisconsin 53201.
Christopher NienhausDepartment of Biomedical Sciences, Marquette University, Milwaukee, Wisconsin 53201.
Murray G BlackmoreDepartment of Biomedical Sciences, Marquette University, Milwaukee, Wisconsin 53201 murray.blackmore@marquette.edu.
Marquette University · US

Funding

Functional Testing of KLF7 in Spinal Cord Injury: An Optogenetic ApproachR01NS083983 · NINDS · MARQUETTE UNIVERSITY · PI BLACKMORE, MURRAY G · 2013 to 2023
$3.5M
NINDS NIH HHS R01 NS083983
6 · The paper itself

Abstract

Embryonic neurons, peripheral neurons, and CNS neurons in zebrafish respond to axon injury by initiating pro-regenerative transcriptional programs that enable axons to extend, locate appropriate targets, and ultimately contribute to behavioral recovery. In contrast, many long-distance projection neurons in the adult mammalian CNS, notably corticospinal tract (CST) neurons, display a much lower regenerative capacity. To promote CNS repair, a long-standing goal has been to activate pro-regenerative mechanisms that are normally missing from injured CNS neurons. Sox11 is a transcription factor whose expression is common to a many types of regenerating neurons, but it is unknown whether suboptimal Sox11 expression contributes to low regenerative capacity in the adult mammalian CNS. Here we show in adult mice that dorsal root ganglion neurons (DRGs) and CST neurons fail to upregulate Sox11 after spinal axon injury. Furthermore, forced viral expression of Sox11 reduces axonal dieback of DRG axons, and promotes CST sprouting and regenerative axon growth in both acute and chronic injury paradigms. In tests of forelimb dexterity, however, Sox11 overexpression in the cortex caused a modest but consistent behavioral impairment. These data identify Sox11 as a key transcription factor that can confer an elevated innate regenerative capacity to CNS neurons. The results also demonstrate an unexpected dissociation between axon growth and behavioral outcome, highlighting the need for additional strategies to optimize the functional output of stimulated neurons.

Indexed as

AdenoviridaeAnimalsDisease Models, AnimalExploratory BehaviorFemaleGanglia, SpinalGene Expression RegulationHand StrengthLuminescent ProteinsMiceMice, Inbred C57BLMice, TransgenicNerve RegenerationNeuronsPsychomotor PerformancePyramidal TractsLuminescent ProteinsSox11 protein, mouseSOXC Transcription Factorsaxon regenerationgene therapySox11spinal cord injurytranscription factor

Identifiers

PMID25698749
PMCPMC4331631
OpenAlexW2084502772

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.