Evidence map›Paper›PMID 25743255›Full record

ArticleNeuroscience2015

Activation of the Wnt/β-catenin signaling cascade after traumatic nerve injury.

S Kurimoto, J Jung, M Tapadia, J Lengfeld, D Agalliu, M Waterman, T Mozaffar, R Gupta

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

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  19. Neuromuscular junction degeneration in muscle wasting.Current opinion in clinical nutrition and metabolic care · 2016
    Review
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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 2 countries.

S KurimotoDepartment of Orthopaedic Surgery, University of California, Irvine, CA 92697, USA; Department of Hand Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya 466-8550, Japan.
J JungDepartment of Orthopaedic Surgery, University of California, Irvine, CA 92697, USA.
M TapadiaDepartment of Orthopaedic Surgery, University of California, Irvine, CA 92697, USA.
J LengfeldDepartment of Developmental and Cell Biology, University of California, Irvine, CA 92697, USA.
D AgalliuDepartment of Developmental and Cell Biology, University of California, Irvine, CA 92697, USA.
M WatermanDepartment of Microbiology and Molecular Genetics, University of California, Irvine, CA 92697, USA.
T MozaffarDepartment of Orthopaedic Surgery, University of California, Irvine, CA 92697, USA; Department of Neurology, University of California, Irvine, CA 92697, USA.
R GuptaDepartment of Orthopaedic Surgery, University of California, Irvine, CA 92697, USA; Department of Biomedical Engineering, University of California, Irvine, CA 92697, USA; Department of Anatomy and Neurobiology, University of California, Irvine, CA 92697, USA. Electronic address: ranjang@uci.edu.
University of California, Irvine · US

Funding

Schwann cell regulation of chronic nerve injuryR01NS049203 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI GUPTA, RANJAN · 2004 to 2014
$3.1M
CNS angiogenesis and blood-brain barrier regulation by the Wnt inhibitor Apcdd1.R01HL116995 · NHLBI · UNIVERSITY OF CALIFORNIA-IRVINE · PI AGALLIU, DRITAN · 2013 to 2017
$1.9M
NHLBI NIH HHS R01 HL116995NINDS NIH HHS 2R01NS049203-06A1NINDS NIH HHS R01 NS049203
6 · The paper itself

Abstract

Recent data have shown that preservation of the neuromuscular junction (NMJ) after traumatic nerve injury helps to improve functional recovery with surgical repair via matrix metalloproteinase-3 (MMP3) blockade. As such, we sought to explore additional pathways that may augment this response. Wnt3a has been shown to inhibit acetylcholine receptor (AChR) clustering via β-catenin-dependent signaling in the development of the NMJ. Therefore, we hypothesized that Wnt3a and β-catenin are associated with NMJ destabilization following traumatic denervation. A critical size nerve defect was created by excising a 10-mm segment of the sciatic nerve in mice. Denervated muscles were then harvested at multiple time points for immunofluorescence staining, quantitative real-time PCR, and western blot analysis for Wnt3a and β-catenin levels. Moreover, a novel Wnt/β-catenin transgenic reporter mouse line was utilized to support our hypothesis of Wnt activation after traumatic nerve injury. The expression of Wnt3a mRNA was significantly increased by 2 weeks post-injury and remained upregulated for 2 months. Additionally, β-catenin was activated at 2 months post-injury relative to controls. Correspondingly, immunohistochemical analysis of denervated transgenic mouse line TCF/Lef:H2B-GFP muscles demonstrated that the number of GFP-positive cells was increased at the motor endplate band. These collective data support that post-synaptic AChRs destabilize after denervation by a process that involves the Wnt/β-catenin pathway. As such, this pathway serves as a potential therapeutic target to prevent the motor endplate degeneration that occurs following traumatic nerve injury.

Indexed as

Muscle DenervationWnt Signaling PathwayAnimalsbeta CateninCell LineMaleMice, 129 StrainMice, TransgenicNeuromuscular JunctionReceptors, CholinergicWnt Proteinsbeta CateninCTNNB1 protein, mouseReceptors, CholinergicWnt Proteinsneuromuscular junctionperipheral nervetraumatic nerve injuryWnt signaling

Identifiers

PMID25743255
PMCPMC5384639
OpenAlexW2062485876

What OpenQuestion holds

Textmetadata
LicenceTDM
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.