Evidence map›Paper›PMID 26130762›Full record

ArticleDiabetes2015

Promoted Interaction of Nuclear Factor-κB With Demethylated Purinergic P2X3 Receptor Gene Contributes to Neuropathic Pain in Rats With Diabetes.

Hong-Hong Zhang, Ji Hu, You-Lang Zhou, Xin Qin, Zhen-Yuan Song, Pan-Pan Yang, Shufen Hu, Xinghong Jiang, Guang-Yin Xu

Abstract read
PubMed Publisher
In one paragraph

Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

50 citing papers in PubMed, 81 citations in OpenAlex.

  1. Trial
  2. Article
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  4. Review
  5. Review
  6. Systematic investigation ofWorld journal of diabetes · 2024
    Article
  7. Review
  8. Metabolic memory: mechanisms and diseases.Signal transduction and targeted therapy · 2024
    Review
  9. The Epigenetics of Neuropathic Pain: A Systematic Update.International journal of molecular sciences · 2023
    Review
  10. Article
  11. FUS Contributes to Nerve Injury-Induced Nociceptive Hypersensitivity by Activating NF-κB Pathway in Primary Sensory Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  12. Article
  13. Identification of a Glutamatergic Claustrum-Anterior Cingulate Cortex Circuit for Visceral Pain Processing.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  14. Article
  15. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Hong-Hong ZhangJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Institute of Neuroscience, The Second Affiliated Hospital, Soochow University, Suzhou, People's Republic of China.
Ji HuJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Institute of Neuroscience, The Second Affiliated Hospital, Soochow University, Suzhou, People's Republic of China guangyinxu@suda.edu.cn huji@suda.edu.cn.
You-Lang ZhouJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Institute of Neuroscience, The Second Affiliated Hospital, Soochow University, Suzhou, People's Republic of China.
Xin QinJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Institute of Neuroscience, The Second Affiliated Hospital, Soochow University, Suzhou, People's Republic of China.
Zhen-Yuan SongJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Institute of Neuroscience, The Second Affiliated Hospital, Soochow University, Suzhou, People's Republic of China.
Pan-Pan YangJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Institute of Neuroscience, The Second Affiliated Hospital, Soochow University, Suzhou, People's Republic of China.
Shufen HuJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Institute of Neuroscience, The Second Affiliated Hospital, Soochow University, Suzhou, People's Republic of China.
Xinghong JiangJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Institute of Neuroscience, The Second Affiliated Hospital, Soochow University, Suzhou, People's Republic of China.
Guang-Yin XuJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Institute of Neuroscience, The Second Affiliated Hospital, Soochow University, Suzhou, People's Republic of China guangyinxu@suda.edu.cn huji@suda.edu.cn.
Second Affiliated Hospital of Soochow University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Painful diabetic neuropathy is a common complication of diabetes produced by mechanisms that as yet are incompletely defined. The aim of this study was to investigate the roles of nuclear factor-κB (NF-κB) in the regulation of purinergic receptor P2X ligand-gated ion channel 3 (P2X3R) plasticity in dorsal root ganglion (DRG) neurons of rats with painful diabetes. Here, we showed that hindpaw pain hypersensitivity in streptozocin-induced diabetic rats was attenuated by treatment with purinergic receptor antagonist suramin or A-317491. The expression and function of P2X3Rs was markedly enhanced in hindpaw-innervated DRG neurons in diabetic rats. The CpG (cytosine guanine dinucleotide) island in the p2x3r gene promoter region was significantly demethylated, and the expression of DNA methyltransferase 3b was remarkably downregulated in DRGs in diabetic rats. The binding ability of p65 (an active form of NF-κB) with the p2x3r gene promoter region and p65 expression were enhanced significantly in diabetes. The inhibition of p65 signaling using the NF-κB inhibitor pyrrolidine dithiocarbamate or recombinant lentiviral vectors designated as lentiviral vector-p65 small interfering RNA remarkably suppressed P2X3R activities and attenuated diabetic pain hypersensitivity. Insulin treatment significantly attenuated pain hypersensitivity and suppressed the expression of p65 and P2X3Rs. Our findings suggest that the p2x3r gene promoter DNA demethylation and enhanced interaction with p65 contributes to P2X3R sensitization and diabetic pain hypersensitivity.

Indexed as

Epigenesis, GeneticAnimalsCpG IslandsDiabetes Mellitus, ExperimentalDiabetic NeuropathiesDNA (Cytosine-5-)-MethyltransferasesDNA MethylationDNA Methyltransferase 3BFemaleGanglia, SpinalGene Expression RegulationHindlimbHypoglycemic AgentsInsulinNerve Tissue ProteinsNeuralgiaDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3BHypoglycemic AgentsInsulinNerve Tissue ProteinsP2rx3 protein, ratPurinergic P2X Receptor AntagonistsReceptors, Purinergic P2X3Rela protein, ratTranscription Factor RelA

Identifiers

PMID26130762
OpenAlexW1908628105

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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.