Evidence map›Paper›PMID 34118948›Full record

ArticleJournal of neuroinflammation2021

miR-1224 contributes to ischemic stroke-mediated natural killer cell dysfunction by targeting Sp1 signaling.

Yan Feng, Yan Li, Ying Zhang, Bo-Hao Zhang, Hui Zhao, Xin Zhao, Fu-Dong Shi, Wei-Na Jin, Xiao-An Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 52 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 4 institutions in 1 country.

Yan Feng *Department of Neurology, Tianjin Medical University General Hospital, Tianjin, China.
Yan Li *Department of Neurology, Tianjin Medical University General Hospital, Tianjin, China.
Ying ZhangDepartment of Neurology, Tianjin Medical University General Hospital, Tianjin, China.
Bo-Hao ZhangThe Third Affiliated Hospital of Zhengzhou University, No. 7 Kangfu front ST, Zhengzhou, Henan, China.
Hui ZhaoDepartment of Neurology, Tianjin Medical University General Hospital, Tianjin, China.
Xin ZhaoThe Third Affiliated Hospital of Zhengzhou University, No. 7 Kangfu front ST, Zhengzhou, Henan, China.
Fu-Dong ShiDepartment of Neurology, Tianjin Medical University General Hospital, Tianjin, China.
Wei-Na JinDepartment of Neurology, Tianjin Medical University General Hospital, Tianjin, China. weina.jin@ncrcnd.org.cn.ORCID http://orcid.org/0000-0002-2196-9078
Xiao-An ZhangThe Third Affiliated Hospital of Zhengzhou University, No. 7 Kangfu front ST, Zhengzhou, Henan, China. zxa@zzu.edu.cn.
Tianjin Medical University General Hospital · CNCapital Medical University · CNThird Affiliated Hospital of Zhengzhou University · CNHenan University of Science and Technology · CN

Funding

National Natural Science Foundation of China 81771274National Natural Science Foundation of China 81971094National Natural Science Foundation of China 91642205
6 · The paper itself

Abstract

backgroundBrain ischemia compromises natural killer (NK) cell-mediated immune defenses by acting on neurogenic and intracellular pathways. Less is known about the posttranscriptional mechanisms that regulate NK cell activation and cytotoxicity after ischemic stroke.

methodsUsing a NanoString nCounter® miRNA array panel, we explored the microRNA (miRNA) profile of splenic NK cells in mice subjected to middle cerebral artery occlusion. Differential gene expression and function/pathway analysis were applied to investigate the main functions of predicted miRNA target genes. miR-1224 inhibitor/mimics transfection and passive transfer of NK cells were performed to confirm the impact of miR-1224 in NK cells after brain ischemia.

resultsWe observed striking dysregulation of several miRNAs in response to ischemia. Among those miRNAs, miR-1224 markedly increased 3 days after ischemic stroke. Transfection of miR-1224 mimics into NK cells resulted in suppression of NK cell activity, while an miR-1224 inhibitor enhanced NK cell activity and cytotoxicity, especially in the periphery. Passive transfer of NK cells treated with an miR-1224 inhibitor prevented the accumulation of a bacterial burden in the lungs after ischemic stroke, suggesting an enhanced immune defense of NK cells. The transcription factor Sp1, which controls cytokine/chemokine release by NK cells at the transcriptional level, is a predicted target of miR-1224. The inhibitory effect of miR-1224 on NK cell activity was blocked in Sp1 knockout mice.

conclusionsThese findings indicate that miR-1224 may serve as a negative regulator of NK cell activation in an Sp1-dependent manner; this mechanism may be a novel target to prevent poststroke infection specifically in the periphery and preserve immune defense in the brain.

Indexed as

Signal TransductionAnimalsBrainDisease Models, AnimalGene Expression ProfilingInfarction, Middle Cerebral ArteryIschemic StrokeKiller Cells, NaturalMagnetic Resonance ImagingMaleMiceMice, Inbred C57BLMicroRNAsSp1 Transcription FactorMicroRNAsMIRN1224 microRNA, mouseSp1 Transcription FactorImmune suppressionIschemic strokemicroRNANatural killer cellsPoststroke infection

Identifiers

PMID34118948
PMCPMC8196447
OpenAlexW3167553775

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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.