Evidence map›Paper›PMID 30980241›Full record

ArticleNeuroscience bulletin2019

Decreased miR-325-5p Contributes to Visceral Hypersensitivity Through Post-transcriptional Upregulation of CCL2 in Rat Dorsal Root Ganglia.

Rui Wu, Ping-An Zhang, Xuelian Liu, Yuan Zhou, Meijie Xu, Xinghong Jiang, Jun Yan, Guang-Yin Xu

Open access · greenAbstract read
In one paragraph

Article in Neuroscience bulletin, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Rui WuCenter for Translational Medicine, Affiliated Zhangjiagang Hospital of Soochow University, Zhangjiagang, 215600, China.
Ping-An ZhangCenter for Translational Medicine, Affiliated Zhangjiagang Hospital of Soochow University, Zhangjiagang, 215600, China.
Xuelian LiuDepartment of Physiology and Neurobiology, Institute of Neuroscience, Soochow University, Suzhou, 215123, China.
Yuan ZhouDepartment of Physiology and Neurobiology, Institute of Neuroscience, Soochow University, Suzhou, 215123, China.
Meijie XuCenter for Translational Medicine, Affiliated Zhangjiagang Hospital of Soochow University, Zhangjiagang, 215600, China.
Xinghong JiangDepartment of Physiology and Neurobiology, Institute of Neuroscience, Soochow University, Suzhou, 215123, China.
Jun YanThe Second Affiliated of Hospital Soochow University, Suzhou, 215004, China.
Guang-Yin XuCenter for Translational Medicine, Affiliated Zhangjiagang Hospital of Soochow University, Zhangjiagang, 215600, China. guangyinxu@suda.edu.cn.
Soochow University · CNZhangjiagang First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic visceral hypersensitivity is an important type of chronic pain with unknown etiology and pathophysiology. Recent studies have shown that epigenetic regulation plays an important role in the development of chronic pain conditions. However, the role of miRNA-325-5p in chronic visceral pain remains unknown. The present study was designed to determine the roles and mechanism of miRNA-325-5p in a rat model of chronic visceral pain. This model was induced by neonatal colonic inflammation (NCI). In adulthood, NCI led to a significant reduction in the expression of miRNA-325-5p in colon-related dorsal root ganglia (DRGs), starting to decrease at the age of 4 weeks and being maintained to 8 weeks. Intrathecal administration of miRNA-325-5p agomir significantly enhanced the colorectal distention (CRD) threshold in a time-dependent manner. NCI also markedly increased the expression of CCL2 (C-C motif chemokine ligand 2) in colon-related DRGs at the mRNA and protein levels relative to age-matched control rats. The expression of CXCL12, IL33, SFRS7, and LGI1 was not significantly altered in NCI rats. CCL2 was co-expressed in NeuN-positive DRG neurons but not in glutamine synthetase-positive glial cells. Furthermore, CCL2 was mainly expressed in isolectin B4-binding- and calcitonin gene-related peptide-positive DRG neurons but in few NF-200-positive cells. More importantly, CCL2 was expressed in miR-325-5p-positive DRG neurons. Intrathecal injection of miRNA-325-5p agomir remarkably reduced the upregulation of CCL2 in NCI rats. Administration of Bindarit, an inhibitor of CCL2, markedly raised the CRD threshold in NCI rats in a dose- and time-dependent manner. These data suggest that NCI suppresses miRNA-325-5p expression and enhances CCL2 expression, thus contributing to visceral hypersensitivity in adult rats.

Indexed as

AnimalsAnimals, NewbornChemokine CCL2ColonGanglia, SpinalHyperalgesiaMaleMicroRNAsRatsRats, Sprague-DawleyTranscription, GeneticUp-RegulationVisceral PainCcl2 protein, ratChemokine CCL2MicroRNAsMIRN325 microRNA, ratCCL2Dorsal root gangliaEpigenetic regulationmiRNA-325-5pVisceral pain

Identifiers

PMID30980241
PMCPMC6754488
OpenAlexW2936644154

What OpenQuestion holds

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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.