Evidence map›Paper›PMID 38713438›Full record

ArticleMolecular neurobiology2024

Transcriptome Analysis Reveals Dynamic Microglial-Induced A1 Astrocyte Reactivity via C3/C3aR/NF-κB Signaling After Ischemic Stroke.

Song Wang, Yuhualei Pan, Chengjie Zhang, Yushang Zhao, Huan Wang, Huixuan Ma, Jinmei Sun, Song Zhang, Jingyi Yao, Dan Xie and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

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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

11 authors.

Song WangExperimental and Translational Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China. biows119@163.com.ORCID http://orcid.org/0000-0002-5447-1815
Yuhualei PanExperimental and Translational Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Chengjie ZhangDepartment of Neurology, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Yushang ZhaoExperimental and Translational Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Huan WangExperimental and Translational Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Huixuan MaDepartment of Neurology, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Jinmei SunDepartment of Neurology, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Song ZhangExperimental and Translational Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Jingyi YaoExperimental and Translational Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Dan XieDepartment of Neurology, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China. danxiedx@126.com.
Yongbo ZhangDepartment of Neurology, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China. yongbozhang@ccmu.edu.cn.

Funding

National Natural Science Foundation of China NO. 82201622Natural Science Foundation of Inner Mongolia NO. 2020MS03017
6 · The paper itself

Abstract

Microglia and astrocytes are key players in neuroinflammation and ischemic stroke. A1 astrocytes are a subtype of astrocytes that are extremely neurotoxic and quickly kill neurons. Although the detrimental A1 astrocytes are present in many neurodegenerative diseases and are considered to accelerate neurodegeneration, their role in the pathophysiology of ischemic stroke is poorly understood. Here, we combined RNA-seq, molecular and immunological techniques, and behavioral tests to investigate the role of A1 astrocytes in the pathophysiology of ischemic stroke. We found that astrocyte phenotypes change from a beneficial A2 type in the acute phase to a detrimental A1 type in the chronic phase following ischemic stroke. The activated microglial IL1α, TNF, and C1q prompt commitment of A1 astrocytes. Inhibition of A1 astrocytes induction attenuates reactive gliosis and ameliorates morphological and functional defects following ischemic stroke. The crosstalk between astrocytic C3 and microglial C3aR contributes to the formation of A1 astrocytes and morphological and functional defects. In addition, NF-κB is activated following ischemic stroke and governs the formation of A1 astrocytes via direct targeting of inflammatory cytokines and chemokines. Taken together, we discovered that A2 astrocytes and A1 astrocytes are enriched in the acute and chronic phases of ischemic stroke respectively, and that the C3/C3aR/NF-κB signaling leads to A1 astrocytes induction. Therefore, the C3/C3aR/NF-κB signaling is a novel therapeutic target for ischemic stroke treatment.

Indexed as

AstrocytesComplement C3Ischemic StrokeMice, Inbred C57BLMicrogliaNF-kappa BSignal TransductionAnimalsGene Expression ProfilingGliosisMaleMiceReceptors, ComplementComplement C3complement C3a receptorNF-kappa BReceptors, ComplementA1 astrocyteC3C3aRIschemic strokeMicrogliaNF-κB

Identifiers

PMID38713438

What OpenQuestion holds

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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.