Evidence map›Paper›PMID 36751804›Full record

ArticleNeural regeneration research2023

Microglia and astrocytes mediate synapse engulfment in a MER tyrosine kinase-dependent manner after traumatic brain injury.

Hui Shen, Xiao-Jing Shi, Lin Qi, Cheng Wang, Muyassar Mamtilahun, Zhi-Jun Zhang, Won-Suk Chung, Guo-Yuan Yang, Yao-Hui Tang

Open access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

9 citing papers in PubMed, 15 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

9 authors at 2 institutions in 2 countries.

Hui ShenMed-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Xiao-Jing ShiMed-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Lin QiMed-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Cheng WangMed-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Muyassar MamtilahunMed-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Zhi-Jun ZhangMed-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Won-Suk ChungDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.
Guo-Yuan YangMed-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Yao-Hui TangMed-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Shanghai Jiao Tong University · CNKorea Advanced Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have shown that microglia/macrophages and astrocytes can mediate synaptic phagocytosis through the MER proto-oncokinase in developmental or stroke models, but it is unclear whether the same mechanism is also active in traumatic brain injury. In this study, we established a mouse model of traumatic brain injury and found that both microglia/macrophages and astrocytes phagocytosed synapses and expression of the MER proto-oncokinase increased 14 days after injury. Specific knockout of MER in microglia/macrophages or astrocytes markedly reduced injury volume and greatly improved neurobehavioral function. In addition, in both microglia/macrophages-specific and astrocytes-specific MER knock-out mice, the number of microglia/macrophage and astrocyte phagocytosing synapses was markedly decreased, and the total number of dendritic spines was increased. Our study suggested that MER proto-oncokinase expression in microglia/macrophages and astrocytes may play an important role in synaptic phagocytosis, and inhibiting this process could be a new strategy for treating traumatic brain injury.

Indexed as

animal modelastrocytedendritic spineslysosomemacrophageMER proto-oncokinasemicroglianeurologic functionphagocytosissynapse engulfmenttraumatic brain injury

Identifiers

PMID36751804
PMCPMC10154480
OpenAlexW4312353515

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.