Evidence map›Paper›PMID 24852102›Full record

ArticleExperimental neurology2014

Chemokine CXCL1 enhances inflammatory pain and increases NMDA receptor activity and COX-2 expression in spinal cord neurons via activation of CXCR2.

De-Li Cao, Zhi-Jun Zhang, Rou-Gang Xie, Bao-Chun Jiang, Ru-Rong Ji, Yong-Jing Gao

Abstract read
In one paragraph

Article in Experimental neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

76 citing papers in PubMed, 125 citations in OpenAlex.

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  13. Redox report : communications in free radical research · 2025
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16 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

6 authors at 3 institutions in 2 countries.

De-Li CaoPain Research Laboratory, Institute of Nautical Medicine, Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Nantong, Jiangsu 226001, China.
Zhi-Jun ZhangPain Research Laboratory, Institute of Nautical Medicine, Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Nantong, Jiangsu 226001, China; Department of Anatomy, Medical School of Nantong University, Nantong, Jiangsu 226001, China.
Rou-Gang XieDepartment of Anesthesiology and Neurobiology, Duke University Medical Center, Durham, NC 27710, USA.
Bao-Chun JiangPain Research Laboratory, Institute of Nautical Medicine, Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Nantong, Jiangsu 226001, China.
Ru-Rong JiDepartment of Anesthesiology and Neurobiology, Duke University Medical Center, Durham, NC 27710, USA.
Yong-Jing GaoPain Research Laboratory, Institute of Nautical Medicine, Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Nantong, Jiangsu 226001, China. Electronic address: gaoyongjing@hotmail.com.
Nantong University · CNDuke Medical Center · USDuke University · US

Funding

Neuronal and glial interactions of neuropathic painR01DE017794 · NIDCR · DUKE UNIVERSITY · PI BUCHHEIT, THOMAS · 2006 to 2021
$6.6M
Hemichannels, Astrocytic Release, and Neuropathic PainR01DE022743 · NIDCR · DUKE UNIVERSITY · PI JI, RU-RONG, NEDERGAARD, MAIKEN · 2012 to 2016
$2.0M
NIDCR NIH HHS DE17794NIDCR NIH HHS DE22743NIDCR NIH HHS R01 DE017794NIDCR NIH HHS R01 DE022743
6 · The paper itself

Abstract

Recent studies have shown that CXCL1 upregulation in spinal astrocytes is involved in the maintenance of neuropathic pain. However, whether and how CXCL1 regulates inflammatory pain remains unknown. Here we show that intraplantar injection of CFA increased mRNA and protein expressions of CXCL1 and its major receptor CXCR2 in the spinal cord at 6h and 3days after the injection. Immunofluorescence double staining showed that CXCL1 and CXCR2 were expressed in spinal astrocytes and neurons, respectively. Intrathecal injection of CXCL1 neutralizing antibody or CXCR2 antagonist SB225002 attenuated CFA-induced mechanical and heat hypersensitivity on post-CFA day 3. Patch-clamp recordings showed that CXCL1 potentiated NMDA-induced currents in lamina II neurons via CXCR2, and this potentiation was further increased in CFA-treated mice. Furthermore, intrathecal injection of CXCL1 increased COX-2 expression in dorsal horn neurons, which was blocked by pretreatment with SB225002 or MEK (ERK kinase) inhibitor PD98059. Finally, pretreatment with SB225002 or PD98059 decreased CFA-induced heat hyperalgesia and COX-2 mRNA/protein expression and ERK activation in the spinal cord. Taken together, our data suggest that CXCL1, upregulated and released by spinal astrocytes after inflammation, acts on CXCR2-expressing spinal neurons to increase ERK activation, synaptic transmission and COX-2 expression in dorsal horn neurons and contributes to the pathogenesis of inflammatory pain.

Indexed as

AnimalsAstrocytesChemokine CXCL1Cyclooxygenase 2Disease Models, AnimalExcitatory Postsynaptic PotentialsFreund's AdjuvantInflammationMaleMembrane PotentialsMiceMice, Inbred ICRNeuronsPainPhenylurea CompoundsPhosphopyruvate HydrataseChemokine CXCL1Cyclooxygenase 2Freund's AdjuvantPhenylurea CompoundsPhosphopyruvate HydratasePtgs2 protein, mouseReceptors, Interleukin-8BReceptors, N-Methyl-D-AspartateSB 225002AstrocytesAstroglial–neuronal interactionChemokinesComplete Freund's adjuvantCOX-2CXCL1CXCR2ERKInflammatory pain

Identifiers

PMID24852102
PMCPMC4194227
OpenAlexW2021889373

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.