Evidence map›Paper›PMID 40673307›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2025

[S1PR5 activation or overexpression enhances barrier function of mouse brain microvascular endothelial cells against OGD/R injury by modulating oxidative stress].

Jingxian Wang, Zijing Ren, Peiyang Zhou

Abstract readEnglish Abstract
In one paragraph

Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Jingxian WangDepartment of Neurology, Xiangyang First People's Hospital, Hubei University of Medicine, Xiangyang 441000, China.
Zijing RenDepartment of Neurology, Xiangyang First People's Hospital, Hubei University of Medicine, Xiangyang 441000, China.
Peiyang ZhouDepartment of Neurology, Xiangyang First People's Hospital, Hubei University of Medicine, Xiangyang 441000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo investigate the role of sphingosine-1-phosphate receptor 5 (S1PR5) in modulating barrier function of mouse brain microvascular endothelial cells with oxygen-glucose deprivation and reoxygenation (OGD/R).

methodsMouse brain microvascular endothelial cells (bEnd.3) were exposed to OGD/R to induce barrier dysfunction following treatment with S1PR5-specific agonist A971432 or lentivirus-mediated transfection with a S1PR5-specific siRNA, a S1PR5-overexpressing plasmid, or their respective negative control sequences. The changes in viability and endothelial barrier permeability of the treated cells were evaluated with CCK-8 assay and FITC-dextran permeability assay; the levels of intracellular reactive oxygen species (ROS) and localization and expression levels of the proteins related with barrier function and oxidative stress were detected using immunofluorescence staining, DCFH-DA probe and Western blotting.

resultsS1PR5 activation obviously enhanced viability of bEnd.3 cells exposed to OGD/R (

conclusionsS1PR5 activation and overexpression significantly improve cell viability and reduce permeability of a mouse brain microvascular endothelial cell model of OGD/R, the mechanism of which may involve the reduction in ROS production and upregulation of the antioxidant proteins.

Indexed as

Blood-Brain BarrierBrainEndothelial CellsOxidative StressReceptors, LysosphingolipidAnimalsCell LineGlucoseMiceNF-E2-Related Factor 2OxygenReactive Oxygen SpeciesSphingosine-1-Phosphate ReceptorsGlucoseNfe2l2 protein, mouseNF-E2-Related Factor 2OxygenReactive Oxygen SpeciesReceptors, LysosphingolipidSphingosine-1-Phosphate Receptorsblood-brain barrier dysfunctionoxidative stressoxygen-glucose deprivation and reoxygenationsphingosine 1-phosphate receptor 5

Identifiers

PMID40673307
PMCPMC12268917

What Socratic holds

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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 Socratic graph.