Evidence map›Paper›PMID 35115050›Full record

ArticleBiological research2022

Neuronal GRK2 regulates microglial activation and contributes to electroacupuncture analgesia on inflammatory pain in mice.

Yu Chen, Yang Zhou, Xiao-Chen Li, Xue Ma, Wen-Li Mi, Yu-Xia Chu, Yan-Qing Wang, Qi-Liang Mao-Ying

Open access · goldAbstract read
In one paragraph

Article in Biological research, 2022. 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
2.9field-weighted citation impact, top 8% 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, 30 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Yu Chen *Department of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, Shanghai Medical College, Institute of Acupuncture Research, Institutes of Integrative Medicine, Fudan University, Shanghai, 200032, People's Republic of China.
Yang Zhou *State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, 200032, People's Republic of China.
Xiao-Chen LiDepartment of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, Shanghai Medical College, Institute of Acupuncture Research, Institutes of Integrative Medicine, Fudan University, Shanghai, 200032, People's Republic of China.
Xue MaDepartment of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, Shanghai Medical College, Institute of Acupuncture Research, Institutes of Integrative Medicine, Fudan University, Shanghai, 200032, People's Republic of China.
Wen-Li MiDepartment of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, Shanghai Medical College, Institute of Acupuncture Research, Institutes of Integrative Medicine, Fudan University, Shanghai, 200032, People's Republic of China.
Yu-Xia ChuDepartment of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, Shanghai Medical College, Institute of Acupuncture Research, Institutes of Integrative Medicine, Fudan University, Shanghai, 200032, People's Republic of China.
Yan-Qing WangDepartment of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, Shanghai Medical College, Institute of Acupuncture Research, Institutes of Integrative Medicine, Fudan University, Shanghai, 200032, People's Republic of China.
Qi-Liang Mao-YingDepartment of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, Shanghai Medical College, Institute of Acupuncture Research, Institutes of Integrative Medicine, Fudan University, Shanghai, 200032, People's Republic of China. maoyql@fudan.edu.cn.
Shanghai Medical College of Fudan University · CNFudan University · CNState Key Laboratory of Medical Neurobiology

Funding

key technologies research and development program 2017YFB0403803national natural science foundation of china 81371247national natural science foundation of china 81473749national natural science foundation of china 81771202national natural science foundation of china 81873101national natural science foundation of china 81971056
6 · The paper itself

Abstract

backgroundG protein coupled receptor kinase 2 (GRK2) has been demonstrated to play a crucial role in the development of chronic pain. Acupuncture is an alternative therapy widely used for pain management. In this study, we investigated the role of spinal neuronal GRK2 in electroacupuncture (EA) analgesia.

methodsThe mice model of inflammatory pain was built by subcutaneous injection of Complete Freund's Adjuvant (CFA) into the plantar surface of the hind paws. The mechanical allodynia of mice was examined by von Frey test. The mice were subjected to EA treatment (BL60 and ST36 acupuncture points) for 1 week. Overexpression and downregulation of spinal neuronal GRK2 were achieved by intraspinal injection of adeno associated virus (AAV) containing neuron-specific promoters, and microglial activation and neuroinflammation were evaluated by real-time PCR.

resultsIntraplantar injection with CFA in mice induced the decrease of GRK2 and microglial activation along with neuroinflammation in spinal cord. EA treatment increased the spinal GRK2, reduced neuroinflammation, and significantly decreased CFA-induced mechanical allodynia. The effects of EA were markedly weakened by non-cell-specific downregulation of spinal GRK2. Further, intraspinal injection of AAV containing neuron-specific promoters specifically downregulated neuronal GRK2, and weakened the regulatory effect of EA on CFA-induced mechanical allodynia and microglial activation. Meanwhile, overexpression of spinal neuronal GRK2 decreased mechanical allodynia. All these indicated that the neuronal GRK2 mediated microglial activation and neuroinflammation, and subsequently contributed to CFA-induced inflammatory pain.

conclusionThe restoration of the spinal GRK2 and subsequent suppression of microglial activation and neuroinflammation might be an important mechanism for EA analgesia. Our findings further suggested that the spinal GRK2, especially neuronal GRK2, might be the potential target for EA analgesia and pain management, and we provided a new experimental basis for the EA treatment of pain.

Indexed as

ElectroacupuncturePain ManagementAnimalsG-Protein-Coupled Receptor Kinase 2InflammationMiceMicrogliaNeuronsPainG-Protein-Coupled Receptor Kinase 2GRK2 protein, mouseElectroacupuncture analgesiaG protein coupled receptor kinase 2Inflammatory painMicroglial activationNeuroinflammation

Identifiers

PMID35115050
PMCPMC8812183
OpenAlexW4210445257

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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.