Evidence map›Paper›PMID 26176363›Full record

ArticleStem cells and development2015

Activation of Type 4 Metabotropic Glutamate Receptor Attenuates Oxidative Stress-Induced Death of Neural Stem Cells with Inhibition of JNK and p38 MAPK Signaling.

Zhichao Zhang, Wen Ma, Li Wang, Hanshi Gong, Yumei Tian, Jianshui Zhang, Jianxin Liu, Haixia Lu, Xinlin Chen, Yong Liu

Abstract read
In one paragraph

Article in Stem cells and development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

12 citing papers in PubMed, 34 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

10 authors at 3 institutions in 1 country.

Zhichao Zhang1 Institute of Neurobiology, Xi'an Jiaotong University Health Science Center , Xi'an, Shaanxi, China .
Wen Ma1 Institute of Neurobiology, Xi'an Jiaotong University Health Science Center , Xi'an, Shaanxi, China .
Li Wang2 Department of Obstetrics and Gynecology, The Affiliated Hospital of Xi'an Medical College , Xi'an, Shaanxi, China .
Hanshi Gong1 Institute of Neurobiology, Xi'an Jiaotong University Health Science Center , Xi'an, Shaanxi, China .
Yumei Tian3 Xi'an Mental Health Center , Xi'an, Shaanxi, China .
Jianshui Zhang1 Institute of Neurobiology, Xi'an Jiaotong University Health Science Center , Xi'an, Shaanxi, China .
Jianxin Liu1 Institute of Neurobiology, Xi'an Jiaotong University Health Science Center , Xi'an, Shaanxi, China .
Haixia Lu1 Institute of Neurobiology, Xi'an Jiaotong University Health Science Center , Xi'an, Shaanxi, China .
Xinlin Chen1 Institute of Neurobiology, Xi'an Jiaotong University Health Science Center , Xi'an, Shaanxi, China .
Yong Liu1 Institute of Neurobiology, Xi'an Jiaotong University Health Science Center , Xi'an, Shaanxi, China .
Xi'an Jiaotong University · CNXi'an Medical University · CNXian Mental Health Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Promoting both endogenous and exogenous neural stem cells' (NSCs) survival in the hostile host environments is essential to cell replacement therapy for central nervous system (CNS) disorders. Type 4 metabotropic glutamate receptor (mGluR4), one of the members of mGluRs, has been shown to protect neurons from acute and chronic excitotoxic insults in various brain damages. The present study investigated the preventive effects of mGluR4 on NSC injury induced by oxidative stress. Under challenge with H2O2, loss of cell viability was observed in cultured rat NSCs, and treatment with selective mGluR4 agonist VU0155041 conferred protective effects against the loss of cellular viability in a concentration-dependent manner, as shown by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Pretreatment of VU0155041 (30 μM) also inhibited the excessive NSC death induced by H2O2, and group III mGluRs antagonist (RS)-a-methylserine-O-phosphate (MSOP) or gene-targeted knockdown abolished the protective action of mGluR4, indicated by propidium iodide-Hoechst and terminal deoxynucleotidyl transferase-mediated UTP nick end labeling (TUNEL) staining. Western blot assay demonstrated that mGluR4 activation reversed the decreased procaspase-8/9/3and the destructed Bcl-2/Bax expressing balance, and likewise, MSOP and mGluR4 knockdown abrogated the action of mGluR4 activity. Furthermore, inhibition of JNK and p38 mitogen-activated protein kinases (MAPKs) were observed after mGluR4 activation, and as paralleling control, JNK-specific inhibitor SP600125 and p38-specific inhibitor SB203580 significantly rescued the H2O2-mediated NSC apoptosis and cleavage of procaspase-3. We suggest that activation of mGluR4 prevents oxidative stress-induced NSC death and apoptotic-associated protein activities with involvement of inhibiting the JNK and p38 pathways in cell culture. Our findings may help to develop strategies for enhancing the resided and transplanted NSC survival after oxidative stress insult of CNS.

Indexed as

ApoptosisMAP Kinase Signaling SystemAnimalsCells, CulturedEmbryonic Stem CellsMAP Kinase Kinase 4Neural Stem CellsOxidative Stressp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsRatsRats, Sprague-DawleyReceptors, Metabotropic GlutamateMAP Kinase Kinase 4metabotropic glutamate receptor 4p38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsReceptors, Metabotropic Glutamate

Identifiers

PMID26176363
PMCPMC4652160
OpenAlexW2209957855

What OpenQuestion holds

Textmetadata
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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.