Evidence map›Paper›PMID 28440797›Full record

ArticleGene therapy2017

Potential mechanisms of microRNA-141-3p to alleviate chronic inflammatory pain by downregulation of downstream target gene HMGB1: in vitro and in vivo studies.

W-S Shen, X-Q Xu, N-N Zhai, Z-S Zhou, J Shao, Y-H Yu

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Gene therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. The role of non-coding RNAs in neuropathic pain.Pflugers Archiv : European journal of physiology · 2024
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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

6 authors at 1 institution in 1 country.

W-S ShenDepartment of Pain Clinic, Shaoxing Traditional Chinese Medical Hospital, Shaoxing, China.
X-Q XuDepartment of Pain Clinic, Shaoxing Traditional Chinese Medical Hospital, Shaoxing, China.
N-N ZhaiDepartment of Pain Clinic, Shaoxing Traditional Chinese Medical Hospital, Shaoxing, China.
Z-S ZhouDepartment of Pain Clinic, Shaoxing Traditional Chinese Medical Hospital, Shaoxing, China.
J ShaoDepartment of Anesthesiology, Shaoxing Traditional Chinese Medical Hospital, Shaoxing, China.
Y-H YuDepartment of Anesthesiology, Shaoxing Traditional Chinese Medical Hospital, Shaoxing, China.
Shaoxing People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study aimed to investigate the potential role of microRNA-141-3p (miR-141-3p) in chronic inflammatory pain (CIP) by targeting the high-mobility group box1 (HMGB1) gene. In the in vitro study, BV2 microglial cells were selected and assigned into blank, lipopolysaccharide (LPS), miR-141-3p mimics, mimics control, miR-141-3p inhibitor, inhibitor control, miR-141-3p mimics+LPS, mimics control+ LPS, miR-141-3p inhibitor+LPS and inhibitor control+LPS groups. Ninety-six rats were randomly divided into 8 groups (12 rats in each group): blank control, model control, negative control (NC), miR-141-3p mimics+ complete Freund's adjuvant (CFA), mimics control+CFA, HMGB1 short hairpin RNA (shRNA)+CFA, HMGB1 NC+CFA and miR-141-3p mimics+HMGB1 shRNA+CFA groups. The quantitative real-time PCR, western blotting, enzyme-linked immunosorbent assay and pain behavioral test were used to measure the miR-141-3p and HMGB1 mRNA expressions, HMGB1 protein expression, inflammatory cytokines levels, and thermal and mechanical pain thresholds, respectively. Compared with the blank, mimics control, inhibitor control and miR-141-3p mimics+LPS groups, the miR-141-3p mimics group had increased miR-141-3p expression and interleukin (IL)-10 levels, and had decreased mRNA and protein expressions of HMGB1 and the levels of IL-1β, tumor necrosis factor-α (TNF-α) and IL-6, whereas the opposite trend were found in the LPS, miR-141-3p inhibitor, mimics control+LPS and inhibitor control+LPS groups. Compared with the LPS, miR-141-3p inhibitor, mimics control+LPS and inhibitor control+LPS groups, the miR141-3p+LPS group had an obviously decreased expression of miR-141-3p and IL-10, increased mRNA and protein expressions of HMGB1 and the levels of IL-1β, TNF-α and IL-6. Compared with the rats in the blank control group, the miR-141-3p expression, IL-10 level, and thermal and mechanical pain thresholds decreased significantly, whereas the mRNA and protein expressions of HMGB1, IL-1β, TNF-α and IL-6 increased significantly in rats in the NC, mimics control+CFA and HMGB1 NC+ CFA groups. The miR-141-3p expression was increased in rats in the miR-141-3p mimics+HMGB1 shRNA+CFA group. Our study demonstrated that miR-141-3p can alleviate the CIP by downregulating the downstream target gene HMGB1.

Indexed as

Down-RegulationAnimalsCell LineChronic PainCytokinesGenetic TherapyHMGB1 ProteinMiceMicroRNAsNeuralgiaPain ThresholdRatsRats, Sprague-DawleyCytokinesHbp1 protein, ratHMGB1 ProteinMicroRNAsMirn141 microRNA, rat

Identifiers

PMID28440797
OpenAlexW2608053089

What OpenQuestion holds

Textmetadata
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.