Evidence map›Paper›PMID 34762231›Full record

ArticleMolecular neurobiology2022

Differential Expression and Distinct Roles of Proteinase-Activated Receptor 2 in Microglia and Neurons in Neonatal Mouse Brain After Hypoxia-Ischemic Injury.

Yicong Liu, Hui Li, Jiangqi Hu, Zhou Wu, Jie Meng, Yoshinori Hayashi, Hiroshi Nakanishi, Hong Qing, Junjun Ni

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 6 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 6 institutions in 2 countries.

Yicong LiuKey Laboratory of Molecular Medicine and Biotherapy, Department of Biology, School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.
Hui LiKey Laboratory of Molecular Medicine and Biotherapy, Department of Biology, School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.
Jiangqi HuDepartment of Prosthodontics, Beijing Stomatological Hospital, School of Stomatology, Capital Medical University, Beijing, 100081, China.
Zhou WuDepartment of Aging Science and Pharmacology, Faculty of Dental Science, Kyushu University, Fukuoka, 812-8582, Japan.
Jie MengDepartment of Neurology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Yoshinori HayashiDepartment of Physiology, Nihon University School of Dentistry, Tokyo, 101-8310, Japan.
Hiroshi NakanishiDepartment of Pharmacology, Faculty of Pharmacy, Yasuda Women's University, Hiroshima, 731-0153, Japan.
Hong QingKey Laboratory of Molecular Medicine and Biotherapy, Department of Biology, School of Life Science, Beijing Institute of Technology, Beijing, 100081, China. hqing@bit.edu.cn.
Junjun NiKey Laboratory of Molecular Medicine and Biotherapy, Department of Biology, School of Life Science, Beijing Institute of Technology, Beijing, 100081, China. nijunjun@bit.edu.cn.ORCID http://orcid.org/0000-0001-8486-8146
Beijing Institute of Technology · CNCapital Medical University · CNKyushu University · JPNihon University · JPSichuan University · CNYasuda Women's University · JP

Funding

beijing institute of technology research fund program 2020CX04166beijing natural science foundation 7212066national natural science foundation of china 32070954zhejiang provincial natural science foundation Q20H140040
6 · The paper itself

Abstract

Regulation of microglial activation and neuroinflammation are critical factors in the pathogenesis of ischemic brain injury. Interest in protease-activated receptor 2 (PAR2) as a pharmaceutical target for various diseases is creasing. However, it is unclear the expression and functions of PAR2 in hypoxia-ischemic (HI) brain injury. Mice with HI and cells with oxygen-glucose deprivation and reoxygenation (OGD/R) were studied. Immunoblot and qRT-PCR were used to study the differential gene expression in cultured microglia and neurons. Immunofluorescent staining was used to study the expression pattern of PAR2 in the HI brain and phagocytotic activity of microglia after OGD/R. In neonatal mice brain after HI, we found PAR2 expression was abundant in neurons, but barely in microglia from the contralateral side of cortex and hippocampus. Conversely, PAR2 expression was barely in neurons while significantly increased in activated microglia from the ipsilateral side of cortex and hippocampus. The activations of PAR2 were increased in both microglia and neuron in a cell model of OGD/R. PAR2 activation mediated the cross-talk between microglia and neurons including the following: microglial PAR2 mediated inflammatory responses that induced neuronal damage; neuronal PAR2 regulated chemokines that recruited activated microglia to damage area; microglia PAR2 controlled the phagocytosis of degenerating neurons. These data suggested differential expression and distinct roles of PAR2 in microglia and neurons after HI injury; thereby, interventions targeting PAR2 may provide insights into the inflammatory-related diseases.

Indexed as

AnimalsAnimals, NewbornBrainCells, CulturedHypoxia-Ischemia, BrainMiceMicrogliaNeuronsReceptor, PAR-2F2rl1 protein, mouseReceptor, PAR-2Hypoxic-ischemic injuryMicrogliaNeuronProtease-activated receptor 2

Identifiers

PMID34762231
OpenAlexW3213675755

What OpenQuestion holds

Textmetadata
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.