Evidence map›Paper›PMID 26781879›Full record

ArticleNeuroscience bulletin2016

Upregulation of Chemokine CXCL12 in the Dorsal Root Ganglia and Spinal Cord Contributes to the Development and Maintenance of Neuropathic Pain Following Spared Nerve Injury in Rats.

Liying Bai, Xinru Wang, Zhisong Li, Cunlong Kong, Yonghui Zhao, Jun-Liang Qian, Quancheng Kan, Wei Zhang, Ji-Tian Xu

Abstract read
In one paragraph

Article in Neuroscience bulletin, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
–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

65 citing papers in PubMed.

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  15. Neuropathic pain; what we know and what we should do about it.Frontiers in pain research (Lausanne, Switzerland) · 2023
    Review
  16. Review
  17. Article
  18. Article
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5 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

9 authors.

Liying BaiDepartment of Physiology and Neurobiology, Zhengzhou University School of Medicine, Zhengzhou, 450001, China.
Xinru WangDepartment of Physiology and Neurobiology, Zhengzhou University School of Medicine, Zhengzhou, 450001, China.
Zhisong LiDepartment of Anesthesiology, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, 450052, China.
Cunlong KongDepartment of Anesthesiology, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, 450052, China.
Yonghui ZhaoDepartment of Anesthesiology, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, 450052, China.
Jun-Liang QianDepartment of Physiology and Neurobiology, Zhengzhou University School of Medicine, Zhengzhou, 450001, China.
Quancheng KanDepartment of Pharmacy, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, 450052, China.
Wei ZhangDepartment of Anesthesiology, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, 450052, China. zhangw571012@126.com.
Ji-Tian XuDepartment of Physiology and Neurobiology, Zhengzhou University School of Medicine, Zhengzhou, 450001, China. jtxu@zzu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence indicates that CXCL12/CXCR4 signaling is involved in chronic pain. However, few studies have systemically assessed its role in direct nerve injury-induced neuropathic pain and the underlying mechanism. Here, we determined that spared nerve injury (SNI) increased the expression of CXCL12 and its cognate receptor CXCR4 in lumbar 5 dorsal root ganglia (DRG) neurons and satellite glial cells. SNI also induced long-lasting upregulation of CXCL12 and CXCR4 in the ipsilateral L4-5 spinal cord dorsal horn, characterized by CXCL12 expression in neurons and microglia, and CXCR4 expression in neurons and astrocytes. Moreover, SNI-induced a sustained increase in TNF-α expression in the DRG and spinal cord. Intraperitoneal injection (i.p.) of the TNF-α synthesis inhibitor thalidomide reduced the SNI-induced mechanical hypersensitivity and inhibited the expression of CXCL12 in the DRG and spinal cord. Intrathecal injection (i.t.) of the CXCR4 antagonist AMD3100, both 30 min before and 7 days after SNI, reduced the behavioral signs of allodynia. Rats given an i.t. or i.p. bolus of AMD3100 on day 8 of SNI exhibited attenuated abnormal pain behaviors. The neuropathic pain established following SNI was also impaired by i.t. administration of a CXCL12-neutralizing antibody. Moreover, repetitive i.t. AMD3100 administration prevented the activation of ERK in the spinal cord. The mechanical hypersensitivity induced in naïve rats by i.t. CXCL12 was alleviated by pretreatment with the MEK inhibitor PD98059. Collectively, our results revealed that TNF-α might mediate the upregulation of CXCL12 in the DRG and spinal cord following SNI, and that CXCL12/CXCR4 signaling via ERK activation contributes to the development and maintenance of neuropathic pain.

Indexed as

AnimalsBlotting, WesternChemokine CXCL12Disease Models, AnimalEnzyme-Linked Immunosorbent AssayGanglia, SpinalHyperalgesiaImmunohistochemistryMaleNeuralgiaNeurogliaNeuronsPeripheral Nerve InjuriesRatsRats, Sprague-DawleySpinal CordChemokine CXCL12CXCL12 protein, ratCXCL12Extracellular signal-regulated kinaseNeuropathic painSpared nerve injurySpinal cordTNF-α

Identifiers

PMID26781879
PMCPMC5563752

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.