Evidence map›Paper›PMID 32171293›Full record

ArticleJournal of neuroinflammation2020

Pellino1 regulates neuropathic pain as well as microglial activation through the regulation of MAPK/NF-κB signaling in the spinal cord.

Lijuan Wang, Cui Yin, Tianya Liu, Mannan Abdul, Yan Zhou, Jun-Li Cao, Chen Lu

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

42 citing papers in PubMed.

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  9. GDF11 Mitigates Neuropathic Pain via Regulation of Microglial Polarization and Neuroinflammation through TGF-βR1/SMAD2/NF-κB Pathway in Male Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
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  12. Neuroplasticity in the transition from acute to chronic pain.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Review
  13. MFG-E8 Ameliorates Nerve Injury-Induced Neuropathic Pain by Regulating Microglial Polarization and Neuroinflammation via Integrin β3/SOCS3/STAT3 Pathway in Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
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  16. Pathology of pain and its implications for therapeutic interventions.Signal transduction and targeted therapy · 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.

Lijuan WangSchool of Anesthesiology, Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical University, Xuzhou, 221002, China.
Cui YinSchool of Anesthesiology, Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical University, Xuzhou, 221002, China.
Tianya LiuSchool of Anesthesiology, Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical University, Xuzhou, 221002, China.
Mannan AbdulSchool of Anesthesiology, Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical University, Xuzhou, 221002, China.
Yan ZhouDepartment of Neurology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou Medical University, Xuzhou, 221002, China.
Jun-Li CaoSchool of Anesthesiology, Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical University, Xuzhou, 221002, China. caojl0310@aliyun.com.
Chen LuSchool of Anesthesiology, Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical University, Xuzhou, 221002, China. lucoct@163.com.

Funding

National Natural Science Foundation of China 81400918National Natural Science Foundation of China 81703493Natural Science Foundation of Jiangsu Province BK20150214Natural Science Foundation of Jiangsu Province BK20170258
6 · The paper itself

Abstract

backgroundSpinal cord microglia plays a crucial role in the pathogenesis of neuropathic pain. However, the mechanisms underlying spinal microglial activation during neuropathic pain remain incompletely determined. Here, we investigated the role of Pellino1 (Peli1) and its interplay with spinal microglial activation in neuropathic pain.

methodsIn this study, we examined the effects of Peli1 on pain hypersensitivity and spinal microglial activation after chronic constriction injury (CCI) of the sciatic nerve in mice. The molecular mechanisms involved in Peli1-mediated hyperalgesia were determined by western blot, immunofluorescence, quantitative polymerase chain reaction (qPCR), and enzyme-linked immunosorbent assay (ELISA). We utilized immunoprecipitation to examine the ubiquitination of tumor necrosis factor receptor-associated factor 6 (TRAF6) following CCI. In addition, we explored the effect of Peli1 on BV2 microglial cells in response to lipopolysaccharide (LPS) challenge.

resultsWe found that CCI induced a significant increase in the levels of Peli1, which was present in the great majority of microglia in the spinal dorsal horn. Our results showed that spinal Peli1 contributed to the induction and maintenance of CCI-induced neuropathic pain. The biochemical data revealed that CCI-induced Peli1 in the spinal cord significantly increased mitogen-activated protein kinase (MAPK) phosphorylation, activated nuclear factor kappa B (NF-κB), and enhanced the production of proinflammatory cytokines, accompanied by spinal microglial activation. Peli1 additionally was able to promote K63-linked ubiquitination of TRAF6 in the ipsilateral spinal cord following CCI. Furthermore, we demonstrated that Peli1 in microglial cells significantly enhanced inflammatory reactions after LPS treatment.

conclusionThese results suggest that the upregulation of spinal Peli1 is essential for the pathogenesis of neuropathic pain via Peli1-dependent mobilization of spinal cord microglia, activation of MAPK/NF-κB signaling, and production of proinflammatory cytokines. Modulation of Peli1 may serve as a potential approach for the treatment of neuropathic pain.

Indexed as

AnimalsMaleMAP Kinase Signaling SystemMiceMicrogliaNeuralgiaNF-kappa BNuclear ProteinsSciatic NerveSignal TransductionSpinal CordUbiquitin-Protein LigasesNF-kappa BNuclear ProteinsPeli1 protein, mouseUbiquitin-Protein LigasesMAPK signalingMicroglial activationNeuroinflammationNeuropathic painNF-κBPellino1

Identifiers

PMID32171293
PMCPMC7071701

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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.