Evidence map›Paper›PMID 34051800›Full record

ArticleJournal of neuroinflammation2021

miR-19a/b-3p promotes inflammation during cerebral ischemia/reperfusion injury via SIRT1/FoxO3/SPHK1 pathway.

Feng Zhou, Yu-Kai Wang, Cheng-Guo Zhang, Bing-Yi Wu

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 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
11.0field-weighted citation impact, top 1% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 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

4 authors at 2 institutions in 1 country.

Feng ZhouResearch Center of Clinical Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong Province, People's Republic of China.
Yu-Kai WangDepartment of Neurology, First People's Hospital of Foshan, Foshan, 528000, Guangdong Province, People's Republic of China.
Cheng-Guo ZhangDepartment of Neurology, First People's Hospital of Foshan, Foshan, 528000, Guangdong Province, People's Republic of China. drzhangcg@163.com.ORCID http://orcid.org/0000-0001-5398-1285
Bing-Yi WuResearch Center of Clinical Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong Province, People's Republic of China. wubingyi66@126.com.
First People's Hospital of Foshan · CNNanfang Hospital · CN

Funding

Medical Science and Technology Foundation of Guangdong Province B2019062National Natural Science Foundation of China 81771340Special Fund of Foshan Summit Plan 2019D044Special Fund of Foshan Summit Plan 2020A022
6 · The paper itself

Abstract

backgroundStroke affects 3-4% of adults and kills numerous people each year. Recovering blood flow with minimal reperfusion-induced injury is crucial. However, the mechanisms underlying reperfusion-induced injury, particularly inflammation, are not well understood. Here, we investigated the function of miR-19a/b-3p/SIRT1/FoxO3/SPHK1 axis in ischemia/reperfusion (I/R).

methodsMCAO (middle cerebral artery occlusion) reperfusion rat model was used as the in vivo model of I/R. Cultured neuronal cells subjected to OGD/R (oxygen glucose deprivation/reperfusion) were used as the in vitro model of I/R. MTT assay was used to assess cell viability and TUNEL staining was used to measure cell apoptosis. H&E staining was employed to examine cell morphology. qRT-PCR and western blot were performed to determine levels of miR-19a/b-3p, SIRT1, FoxO3, SPHK1, NF-κB p65, and cytokines like TNF-α, IL-6, and IL-1β. EMSA and ChIP were performed to validate the interaction of FoxO3 with SPHK1 promoter. Dual luciferase assay and RIP were used to verify the binding of miR-19a/b-3p with SIRT1 mRNA.

resultsmiR-19a/b-3p, FoxO3, SPHK1, NF-κB p65, and cytokines were elevated while SIRT1 was reduced in brain tissues following MCAO/reperfusion or in cells upon OGD/R. Knockdown of SPHK1 or FoxO3 suppressed I/R-induced inflammation and cell death. Furthermore, knockdown of FoxO3 reversed the effects of SIRT1 knockdown. Inhibition of the miR-19a/b-3p suppressed inflammation and this suppression was blocked by SIRT1 knockdown. FoxO3 bound SPHK1 promoter and activated its transcription. miR-19a/b-3p directly targeted SIRT1 mRNA.

conclusionmiR-19a/b-3p promotes inflammatory responses during I/R via targeting SIRT1/FoxO3/SPHK1 axis.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosisCell DeathCell LineDisease Models, AnimalForkhead Box Protein O3Gene Knockdown TechniquesHumansInfarction, Middle Cerebral ArteryInflammationMaleMicroRNAsPhosphotransferases (Alcohol Group Acceptor)RatsRats, Sprague-DawleyAdaptor Proteins, Signal TransducingForkhead Box Protein O3MicroRNAsMIRN19A microRNA, humanMIRN19 microRNA, ratPhosphotransferases (Alcohol Group Acceptor)Sirtuin 1FoxO3InflammationIschemiamiR-19a/b-3pSIRT1SPHK1

Identifiers

PMID34051800
PMCPMC8164774
OpenAlexW3165197804

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.