Evidence map›Paper›PMID 33167866›Full record

ArticleMolecular medicine (Cambridge, Mass.)2020

Downregulation of long noncoding RNA DLEU1 attenuates hypersensitivity in chronic constriction injury-induced neuropathic pain in rats by targeting miR-133a-3p/SRPK1 axis.

Zhen Li, Aiyuan Li, Liping Yan, Tian Yang, Wei Xu, Pengju Fan

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2020. 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
0.9field-weighted citation impact, top 31% 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, 20 citations in OpenAlex.

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  9. Research progress on long non-coding RNAs for spinal cord injury.Journal of orthopaedic surgery and research · 2023
    Review
  10. Article
  11. DNA Methylation and Non-Coding RNAs during Tissue-Injury Associated Pain.International journal of molecular sciences · 2022
    Review
  12. Article
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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 2 institutions in 1 country.

Zhen LiDepartment of Anesthesiology, Hunan Provincial Maternal and Child Health Care Hospital, Changsha, 410008, Hunan, China.
Aiyuan LiDepartment of Anesthesiology, Hunan Provincial Maternal and Child Health Care Hospital, Changsha, 410008, Hunan, China.
Liping YanDepartment of Anesthesiology, Hunan Provincial Maternal and Child Health Care Hospital, Changsha, 410008, Hunan, China.
Tian YangDepartment of Anesthesiology, Hunan Provincial Maternal and Child Health Care Hospital, Changsha, 410008, Hunan, China.
Wei XuDepartment of Anesthesiology, Hunan Provincial Maternal and Child Health Care Hospital, Changsha, 410008, Hunan, China.
Pengju FanDepartment of Burn and Plastic Surgery, Xiangya Hospital Central South University, No. 87 Xiangya Road, Kaifu District, Changsha, 410008, Hunan, China. fanpengju2020@hotmail.com.ORCID 0000-0001-6593-8663
Hunan Provincial Maternal and Child Health Hospital · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuropathic pain belongs to chronic pain and is caused by the primary dysfunction of the somatosensory nervous system. Long noncoding RNAs (lncRNAs) have been reported to regulate neuronal functions and play significant roles in neuropathic pain. DLEU1 has been indicated to have close relationship with neuropathic pain. Therefore, our study focused on the significant role of DLEU1 in neuropathic pain rat models.

methodsWe first constructed a chronic constrictive injury (CCI) rat model. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were employed to evaluate hypersensitivity in neuropathic pain. RT-qPCR was performed to analyze the expression of target genes. Enzyme-linked immunosorbent assay (ELISA) was conducted to detect the concentrations of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and IL-1β. The underlying mechanisms of DLEU1 were investigated using western blot and luciferase reporter assays.

resultsOur findings showed that DLEU1 was upregulated in CCI rats. DLEU1 knockdown reduced the concentrations of IL-6, IL-1β and TNF-α in CCI rats, suggesting that neuroinflammation was inhibited by DLEU1 knockdown. Besides, knockdown of DLEU1 inhibited neuropathic pain behaviors. Moreover, it was confirmed that DLEU1 bound with miR-133a-3p and negatively regulated its expression. SRPK1 was the downstream target of miR-133a-3p. DLEU1 competitively bound with miR-133a-3p to upregulate SRPK1. Finally, rescue assays revealed that SRPK1 overexpression rescued the suppressive effects of silenced DLEU1 on hypersensitivity in neuropathic pain and inflammation of spinal cord in CCI rats.

conclusionDLEU1 regulated inflammation of the spinal cord and mediated hypersensitivity in neuropathic pain in CCI rats by binding with miR-133a-3p to upregulate SRPK1 expression.

Indexed as

Gene Expression RegulationPain ThresholdRNA InterferenceAnimalsBiomarkersCytokinesDisease Models, AnimalFemaleGene Knockdown TechniquesInflammation MediatorsMicroRNAsNeuralgiaProtein Serine-Threonine KinasesRatsRNA, Long NoncodingSpinal CordBiomarkersCytokinesInflammation MediatorsMicroRNAsMIRN133 microRNA, ratProtein Serine-Threonine KinasesRNA, Long NoncodingSrpk1 protein, ratDLEU1miR-133a-3pNeuropathic painSRPK1

Identifiers

PMID33167866
PMCPMC7653812
OpenAlexW3102387087

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LicenceCC BY
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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.