Evidence map›Paper›PMID 37138283›Full record

ArticleJournal of translational medicine2023

Neuropilin-1 promotes mitochondrial structural repair and functional recovery in rats with cerebral ischemia.

Ting Guo, Manli Chen, Ji Liu, Zengyu Wei, Jinjin Yuan, Wenwen Wu, Zhiyun Wu, Yongxing Lai, Zijun Zhao, Hongbin Chen and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

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  19. Cognitive Impairment in Multiple Sclerosis.Bioengineering (Basel, Switzerland) · 2023
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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 at 1 institution in 1 country.

Ting Guo *Department of Neurology, Fujian Medical University Union Hospital, Fuzhou, China.
Manli Chen *Department of Neurology, Fujian Medical University Union Hospital, Fuzhou, China.
Ji Liu *Department of Neurology, Fujian Medical University Union Hospital, Fuzhou, China.
Zengyu WeiEmergency Department, Fujian Medical University Union Hospital, Fuzhou, China.
Jinjin YuanDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, China.
Wenwen WuDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, China.
Zhiyun WuDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, China.
Yongxing LaiDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, China.
Zijun ZhaoDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, China.
Hongbin ChenDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, China. hbchen0127@fjmu.edu.cn.
Nan LiuDepartment of Neurology, Fujian Medical University Union Hospital, Fuzhou, China. xieheliunan1984@sina.com.ORCID 0000-0003-2901-3721
Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesAvailable literature documents that ischemic stroke can disrupt the morphology and function of mitochondria and that the latter in other disease models can be preserved by neuropilin-1 (NRP-1) via oxidative stress suppression. However, whether NRP-1 can repair mitochondrial structure and promote functional recovery after cerebral ischemia is still unknown. This study tackled this very issue and explored the underlying mechanism.

methodsAdeno-associated viral (AAV)-NRP-1 was stereotaxically inoculated into the cortex and ipsilateral striatum posterior of adult male Sprague-Dawley (SD) rats before a 90-min transient middle cerebral artery occlusion (tMCAO) and subsequent reperfusion. Lentivirus (LV)-NRP-1 was transfected into rat primary cortical neuronal cultures before a 2-h oxygen-glucose deprivation and reoxygenation (OGD/R) injury to neurons. The expression and function of NRP-1 and its specific protective mechanism were investigated by Western Blot, immunofluorescence staining, flow cytometry, magnetic resonance imaging, transmission electron microscopy, etc. The binding was detected by molecular docking and molecular dynamics simulation.

resultsBoth in vitro and in vivo models of cerebral ischemia/reperfusion (I/R) injury presented a sharp increase in NRP-1 expression. The expression of AAV-NRP-1 markedly ameliorated the cerebral I/R-induced damage to the motor function and restored the mitochondrial morphology. The expression of LV-NRP-1 alleviated mitochondrial oxidative stress and bioenergetic deficits. AAV-NRP-1 and LV-NRP-1 treatments increased the wingless integration (Wnt)-associated signals and β-catenin nuclear localization. The protective effects of NRP-1 were reversed by the administration of XAV-939.

conclusionsNRP-1 can produce neuroprotective effects against I/R injury to the brain by activating the Wnt/β-catenin signaling pathway and promoting mitochondrial structural repair and functional recovery, which may serve as a promising candidate target in treating ischemic stroke.

Indexed as

Brain IschemiaIschemic StrokeNeuroprotective AgentsReperfusion InjuryAnimalsApoptosisInfarction, Middle Cerebral ArteryMaleMitochondriaMolecular Docking SimulationNeuropilin-1RatsRats, Sprague-DawleyNeuropilin-1Neuroprotective AgentsIschemia/reperfusionMitochondrial structure and functionNeuronal apoptosisNRP-1Oxidative stress

Identifiers

PMID37138283
PMCPMC10155168
OpenAlexW4368356525

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.