Evidence map›Paper›PMID 32248399›Full record

ArticleNeurochemical research2020

Long Noncoding RNA SNHG5 Knockdown Alleviates Neuropathic Pain by Targeting the miR-154-5p/CXCL13 Axis.

Mi Chen, Yang Yang, Wenqi Zhang, Xinning Li, Jinli Wu, Xiaohua Zou, Xianggang Zeng

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  4. CXCL13/CXCR5: a new target for pain treatment.International journal of surgery (London, England) · 2025
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  6. The role of non-coding RNAs in neuropathic pain.Pflugers Archiv : European journal of physiology · 2024
    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

7 authors at 2 institutions in 1 country.

Mi ChenDepartment of Anesthesiology, Affiliated Hospital of Guizhou Medical University, Guizhou Province, No. 28 Guiyi Street, Guiyang, 550004, China.
Yang YangDepartment of Anesthesiology, Affiliated Hospital of Guizhou Medical University, Guizhou Province, No. 28 Guiyi Street, Guiyang, 550004, China.
Wenqi ZhangDepartment of Anesthesiology, Affiliated Hospital of Guizhou Medical University, Guizhou Province, No. 28 Guiyi Street, Guiyang, 550004, China.
Xinning LiCollege of Anesthesia, Guizhou Medical University, Guizhou Province, Guiyang, 550004, China.
Jinli WuDepartment of Anesthesiology, Affiliated Hospital of Guizhou Medical University, Guizhou Province, No. 28 Guiyi Street, Guiyang, 550004, China.
Xiaohua ZouDepartment of Anesthesiology, Affiliated Hospital of Guizhou Medical University, Guizhou Province, No. 28 Guiyi Street, Guiyang, 550004, China. anesch@163.com.
Xianggang ZengDepartment of Anesthesiology, Affiliated Hospital of Guizhou Medical University, Guizhou Province, No. 28 Guiyi Street, Guiyang, 550004, China. XianggangZengfhj@163.com.
Guiyang Medical University · CNAffiliated Hospital of Guizhou Medical University · CN

Funding

Innovation and Entrepreneurship Training Program for College Students in Guizhou Province 20195200924
6 · The paper itself

Abstract

Neuropathic pain is an unneglectable pain condition with limited treatment options owing to its enigmatic underlying mechanisms. Long noncoding RNA small nucleolar RNA host gene 5 (SNHG5) is involved in the progression of a spectrum of human cancers. However, its role in neuropathic pain remains undiscovered. In the present study, we established a mouse spinal nerve ligation (SNL) model, and a significant upregulation of SNHG5 was observed. Then we knocked down SNHG5 level in mouse L5 dorsal root ganglion (DRG) by delivering specific short hairpin RNA against SNHG5 with adenovirus vehicle. Mouse paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) in response to mechanical stimuli was increased after SNHG5 knockdown, accompanied with decreased protein levels of glial fibrillary acidic protein (GFAP) and ionized calcium binding adapter molecule 1 (IBA-1). Besides, SNHG5 directly modulated the expression of miR-154-5p, which was downregulated in SNL mice. MiR-154-5p inhibition abolished the effect of SNHG5 knockdown on mouse behavioral tests and GFAP and IBA-1 levels. In addition, we validated that C-X-C motif chemokine 13 (CXCL13) was a novel downstream target of miR-154-5p, and CXCL13 level was positively related to that of SNHG5 in SNL mice. In conclusion, our study demonstrated that SNHG5 knockdown alleviated neuropathic pain and inhibited the activation of astrocytes and microglia by targeting the miR-154-5p/CXCL13 axis, which might be a novel therapeutic target for neuropathic treatment clinically.

Indexed as

AdenoviridaeAnimalsChemokine CXCL13Gene Knockdown TechniquesHEK293 CellsHumansMaleMiceMice, Inbred C57BLMicroRNAsNeuralgiaRNA, Long NoncodingChemokine CXCL13Cxcl13 protein, mouselong non-coding RNA SNHG5, humanMicroRNAsMIRN154 microRNA, mouseRNA, Long NoncodingCXCL13miR-154-5pNeuropathic painSNHG5

Identifiers

PMID32248399
OpenAlexW3014264837

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.