Evidence map›Paper›PMID 33070779›Full record

ArticleJournal of neuroinflammation2020

NFATc2-dependent epigenetic upregulation of CXCL14 is involved in the development of neuropathic pain induced by paclitaxel.

Meng Liu, Su-Bo Zhang, Yu-Xuan Luo, Yan-Ling Yang, Xiang-Zhong Zhang, Bo Li, Yan Meng, Yuan-Jie Chen, Rui-Xian Guo, Yuan-Chang Xiong and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. [Temporal changes of chronic postsurgical pain in mice: the regulatory role of CX3CL1 in the dorsal root ganglion].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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  5. Review
  6. Inhibition of NFAT5-Dependent Astrocyte Swelling Alleviates Neuropathic Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
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  8. 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

12 authors at 5 institutions in 1 country.

Meng LiuNeuroscience Program, The Fifth Affiliated Hospital of Sun Yat-Sen University, Guangdong Province Key Laboratory of Brain Function and Disease, Sun Yat-Sen University, Guangzhou, 510080, China.
Su-Bo ZhangNeuroscience Program, The Fifth Affiliated Hospital of Sun Yat-Sen University, Guangdong Province Key Laboratory of Brain Function and Disease, Sun Yat-Sen University, Guangzhou, 510080, China.
Yu-Xuan LuoDepartment of Hematology, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510630, China.
Yan-Ling YangDepartment of Hematology, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510630, China.
Xiang-Zhong ZhangDepartment of Hematology, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510630, China.
Bo LiDepartment of Anesthesiology, Changhai Hospital, Naval Medical University, 168 Changhai Road, Shanghai, 200433, China.
Yan MengDepartment of Anesthesiology, Changhai Hospital, Naval Medical University, 168 Changhai Road, Shanghai, 200433, China.
Yuan-Jie ChenDepartment of Anesthesiology, Changhai Hospital, Naval Medical University, 168 Changhai Road, Shanghai, 200433, China.
Rui-Xian GuoNeuroscience Program, The Fifth Affiliated Hospital of Sun Yat-Sen University, Guangdong Province Key Laboratory of Brain Function and Disease, Sun Yat-Sen University, Guangzhou, 510080, China. guorx@mail.sysu.edu.cn.
Yuan-Chang XiongDepartment of Anesthesiology, Changhai Hospital, Naval Medical University, 168 Changhai Road, Shanghai, 200433, China.
Wen-Jun XinNeuroscience Program, The Fifth Affiliated Hospital of Sun Yat-Sen University, Guangdong Province Key Laboratory of Brain Function and Disease, Sun Yat-Sen University, Guangzhou, 510080, China.
Dai LiDepartment of Anesthesiology, Changhai Hospital, Naval Medical University, 168 Changhai Road, Shanghai, 200433, China. lidaichhosp@163.com.
Changhai Hospital · CNSun Yat-sen University · CNFifth Affiliated Hospital of Sun Yat-sen University · CNSecond Military Medical University · CNThird Affiliated Hospital of Sun Yat-sen University · CN

Funding

National Natural Science Foundation of China 81600955National Natural Science Foundation of China 81971048Natural Science Foundation of Guangdong Province 2017A030313132Natural Science Foundation of Guangdong Province 2020A1515011306Natural Science Foundation of Shanghai 17ZR1438200Scientific Research Program of Shanghai Health and Family Planning Commission 201540128Scientific Research Program of Shanghai Municipal Health Commission 201940512
6 · The paper itself

Abstract

backgroundThe major dose-limiting toxicity of paclitaxel, one of the most commonly used drugs to treat solid tumor, is painful neuropathy. However, the molecular mechanisms underlying paclitaxel-induced painful neuropathy are largely unclarified.

methodsPaw withdrawal threshold was measured in the rats following intraperitoneal injection of paclitaxel. The qPCR, western blotting, protein or chromatin immunoprecipitation, ChIP-seq identification of NFATc2 binding sites, and microarray analysis were performed to explore the molecular mechanism.

resultsWe found that paclitaxel treatment increased the nuclear expression of NFATc2 in the spinal dorsal horn, and knockdown of NFATc2 with NFATc2 siRNA significantly attenuated the mechanical allodynia induced by paclitaxel. Further binding site analysis utilizing ChIP-seq assay combining with gene expression profile revealed a shift of NFATc2 binding site closer to TTS of target genes in dorsal horn after paclitaxel treatment. We further found that NFATc2 occupancy may directly upregulate the chemokine CXCL14 expression in dorsal horn, which was mediated by enhanced interaction between NFATc2 and p300 and consequently increased acetylation of histone H4 in CXCL14 promoter region. Also, knockdown of CXCL14 in dorsal horn significantly attenuated mechanical allodynia induced by paclitaxel.

conclusionThese results suggested that enhanced interaction between p300 and NFATc2 mediated the epigenetic upregulation of CXCL14 in the spinal dorsal horn, which contributed to the chemotherapeutic paclitaxel-induced chronic pain.

Indexed as

AnimalsAntineoplastic Agents, PhytogenicBase SequenceChemokines, CXCEpigenesis, GeneticMaleNeuralgiaNFATC Transcription FactorsPaclitaxelProtein BindingRatsRats, Sprague-DawleyUp-RegulationAntineoplastic Agents, PhytogenicChemokines, CXCCXCL14 protein, ratNFATC Transcription FactorsPaclitaxelCXCL14Histone acetylationNeuropathic painNFATc2Paclitaxel

Identifiers

PMID33070779
PMCPMC7570122
OpenAlexW3093019074

What OpenQuestion holds

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LicenceCC BY
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.