Evidence map›Paper›PMID 32446302›Full record

ArticleJournal of neuroinflammation2020

Expression profiling of spinal cord dorsal horn in a rat model of complex regional pain syndrome type-I uncovers potential mechanisms mediating pain and neuroinflammation responses.

Ruixiang Chen, Chengyu Yin, Qimiao Hu, Boyu Liu, Yan Tai, Xiaoli Zheng, Yuanyuan Li, Jianqiao Fang, Boyi Liu

Open access · goldAbstract 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 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
8.9field-weighted citation impact, top 1% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.

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  19. Neuropathogenesis of HIV and emerging therapeutic targets.Expert opinion on therapeutic targets · 2022
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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

9 authors at 2 institutions in 1 country.

Ruixiang ChenDepartment of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, 548 Binwen Road, Hangzhou, 310053, China.
Chengyu YinDepartment of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, 548 Binwen Road, Hangzhou, 310053, China.
Qimiao HuDepartment of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, 548 Binwen Road, Hangzhou, 310053, China.
Boyu LiuDepartment of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, 548 Binwen Road, Hangzhou, 310053, China.
Yan TaiAcademy of Chinese Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Xiaoli ZhengDepartment of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, 548 Binwen Road, Hangzhou, 310053, China.
Yuanyuan LiDepartment of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, 548 Binwen Road, Hangzhou, 310053, China.
Jianqiao FangDepartment of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, 548 Binwen Road, Hangzhou, 310053, China. fangjianqiao7532@163.com.
Boyi LiuDepartment of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, 548 Binwen Road, Hangzhou, 310053, China. boyi.liu@foxmail.com.ORCID http://orcid.org/0000-0001-9870-4548
The Third Affiliated Hospital of Zhejiang Chinese Medical University · CNZhejiang Chinese Medical University · CN

Funding

National Natural Science Foundation of China 81603676National Natural Science Foundation of China 81873365Research funds from Zhejiang Chinese Medical University 2018ZY19Research funds from Zhejiang Chinese Medical University 2018ZY37Research funds from Zhejiang Chinese Medical University Q2019J01Zhejiang Province Top Discipline of Chinese Medicine ZTK2017A03Zhejiang Province Top Discipline of Chinese Medicine ZTK2017A04Zhejiang Provincial Natural Science Funds for Distinguished Young Scholars LR17H270001
6 · The paper itself

Abstract

backgroundComplex regional pain syndrome type-I (CRPS-I) is a progressive and devastating pain condition. The mechanisms of CRPS-I still remain poorly understood. We aim to explore expression profiles of genes relevant to pain and neuroinflammation mechanisms involved in CRPS-I.

methodsThe rat chronic post-ischemic pain (CPIP) model that mimics human CRPS-I was established. RNA-sequencing (RNA-Seq), qPCR, Western blot, immunostaining, and pharmacological studies were used for profiling gene changes in ipsilateral spinal cord dorsal horn (SCDH) of CPIP model rat and further validation.

resultsCPIP rats developed persistent mechanical allodynia in bilateral hind paws, accompanied with obvious glial activation in SCDH. RNA-Seq identified a total of 435 differentially expressed genes (DEGs) in ipsilateral SCDH of CPIP rats. qPCR confirmed the expression of several representative genes. Functional analysis of DEGs identified that the most significantly enriched biological processes of upregulated genes include inflammatory and innate immune response. We further identified NLRP3 inflammasome expression to be significantly upregulated in SCDH of CPIP rats. Pharmacological blocking NLRP3 inflammasome reduced IL-1β overproduction, glial activation in SCDH as well as mechanical allodynia of CPIP rats.

conclusionOur study revealed that immune and inflammatory responses are predominant biological events in SCDH of CPIP rats. We further identified NLRP3 inflammasome in SCDH as a key contributor to the pain and inflammation responses in CPIP rats. Thus, our study provided putative novel targets that may help to develop effective therapeutics against CRPS-I.

Indexed as

AnimalsDisease Models, AnimalGene Expression ProfilingInflammasomesInflammationMaleNLR Family, Pyrin Domain-Containing 3 ProteinPainRatsRats, Sprague-DawleyReflex Sympathetic DystrophySpinal Cord Dorsal HornInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratCRPS-ICytokineInflammasomeInflammationPainRNA-SeqSpinal cord dorsal horn

Identifiers

PMID32446302
PMCPMC7245895
OpenAlexW3027271186

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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.