Evidence map›Paper›PMID 39592234›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2025

H3K27 Trimethylation-Mediated Downregulation of miR-216a-3p in Sensory Neurons Regulates Neuropathic Pain Behaviors via Targeting STIM1.

Yufang Sun, Yu Tao, Junping Cao, Yaqun Zhang, Zitong Huang, Shoupeng Wang, Weiwei Lu, Qi Zhu, Lidong Shan, Dongsheng Jiang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Epigenetic Repression of miR-216a-3p via H3K27me3 Drives STIM1-Mediated Neuronal Excitability in Neuropathic Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  3. Review
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.

Yufang SunDepartment of Geriatrics, Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou 215004, China.
Yu TaoDepartment of Physiology and Neurobiology, Centre for Ion Channelopathy, Suzhou Medical College of Soochow University, Suzhou 215123, China.
Junping CaoJiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical University, Xuzhou 221004, China.
Yaqun ZhangDepartment of Physiology and Neurobiology, Centre for Ion Channelopathy, Suzhou Medical College of Soochow University, Suzhou 215123, China.
Zitong HuangDepartment of Physiology and Neurobiology, Centre for Ion Channelopathy, Suzhou Medical College of Soochow University, Suzhou 215123, China.
Shoupeng WangDepartment of Physiology and Neurobiology, Centre for Ion Channelopathy, Suzhou Medical College of Soochow University, Suzhou 215123, China.ORCID 0000-0001-8578-2133
Weiwei LuDepartment of Physiology and Neurobiology, Centre for Ion Channelopathy, Suzhou Medical College of Soochow University, Suzhou 215123, China.
Qi ZhuDepartment of Physiology and Neurobiology, Centre for Ion Channelopathy, Suzhou Medical College of Soochow University, Suzhou 215123, China.
Lidong ShanDepartment of Physiology and Neurobiology, Centre for Ion Channelopathy, Suzhou Medical College of Soochow University, Suzhou 215123, China.
Dongsheng JiangPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China.
Yuan ZhangDepartment of Geriatrics, Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou 215004, China taoj@suda.edu.cn yuanzhang@suda.edu.cn.
Jin TaoDepartment of Physiology and Neurobiology, Centre for Ion Channelopathy, Suzhou Medical College of Soochow University, Suzhou 215123, China taoj@suda.edu.cn yuanzhang@suda.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the therapeutic potential of microRNA-mediated gene regulation has been investigated, its precise functional regulatory mechanism in neuropathic pain remains incompletely understood. In this study, we elucidate that miR-216a-3p serves as a critical noncoding RNA involved in the modulation of trigeminal-mediated neuropathic pain. By conducting RNA-seq and qPCR analysis, we observed a notable decrease of miR-216a-3p in the injured trigeminal ganglia (TG) of male rats. Intra-TG administration of miR-216a-3p agomir or lentiviral-mediated overexpression of miR-216a-3p specifically in sensory neurons of injured TGs alleviated established neuropathic pain behaviors, while downregulation of miR-216a-3p (pharmacologically or genetically) in naive rats induced pain behaviors. Moreover, nerve injury significantly elevated the histone H3 lysine-27 (H3K27) trimethylation (H3K27me3) levels in the ipsilateral TG, thereby suppressing the SRY-box TF 10 (SOX10) binding to the

Indexed as

Down-RegulationHistonesMicroRNAsNeuralgiaRats, Sprague-DawleySensory Receptor CellsStromal Interaction Molecule 1AnimalsHistone-Lysine N-MethyltransferaseMaleMethylationRatsHistone-Lysine N-MethyltransferaseHistonesMicroRNAsStim1 protein, ratStromal Interaction Molecule 1histone methylationmiR-216a-3pneuropathic painstromal interaction molecule 1trigeminal ganglion neurons

Identifiers

PMID39592234
PMCPMC11694406

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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.