Evidence map›Paper›PMID 29500411›Full record

ArticleCell death & disease2018

Astrocytic JWA deletion exacerbates dopaminergic neurodegeneration by decreasing glutamate transporters in mice.

Rihua Wang, Xue Zhao, Jin Xu, Yifan Wen, Aiping Li, Ming Lu, Jianwei Zhou

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

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  14. International journal of biological sciences · 2022
    Article
  15. Review
  16. The Potential Role of Astrocytes in Parkinson's Disease (PD).Medical sciences (Basel, Switzerland) · 2020
    Review
  17. Review
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

7 authors at 1 institution in 1 country.

Rihua WangDepartemnt of Molecular Cell Biology & Toxicology, School of Public Health, Nanjing Medical University, 101 Lonamian Avenue, Jiangning District, Nanjing, 211166, China.
Xue ZhaoDepartemnt of Molecular Cell Biology & Toxicology, School of Public Health, Nanjing Medical University, 101 Lonamian Avenue, Jiangning District, Nanjing, 211166, China.
Jin XuDepartemnt of Molecular Cell Biology & Toxicology, School of Public Health, Nanjing Medical University, 101 Lonamian Avenue, Jiangning District, Nanjing, 211166, China.
Yifan WenDepartemnt of Molecular Cell Biology & Toxicology, School of Public Health, Nanjing Medical University, 101 Lonamian Avenue, Jiangning District, Nanjing, 211166, China.
Aiping LiDepartemnt of Molecular Cell Biology & Toxicology, School of Public Health, Nanjing Medical University, 101 Lonamian Avenue, Jiangning District, Nanjing, 211166, China.
Ming LuNeuroprotective Drug Discovery Key Laboratory, Department of Pharmacology, Nanjing Medical University, 101 Longmian Avenue, Jiangning District, Nanjing, 211166, China. lum@njmu.edu.cn.
Jianwei ZhouDepartemnt of Molecular Cell Biology & Toxicology, School of Public Health, Nanjing Medical University, 101 Lonamian Avenue, Jiangning District, Nanjing, 211166, China. jwzhou@njmu.edu.cn.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Astrocytic JWA exerts neuroprotective roles by alleviating oxidative stress and inhibiting inflammation. However, the molecular mechanisms of how astrocytic JWA is involved in dopaminergic neurodegeneration in Parkinson's disease (PD) remain largely unknown. In this study, we found that astrocyte-specific JWA knockout mice (JWA CKO) exacerbated dopamine (DA) neuronal loss and motor dysfunction, and reduced the levels of DA and its metabolites in a 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine/probenecid (MPTP/p)-induced PD model. Astrocytic JWA deficiency repressed expression of excitatory amino-acid transporter 2 (GLT-1) and glutamate uptake both in vivo and in vitro. Further, the regulation of GLT-1 expression was involved in JWA-triggered activation of the MAPK and PI3K signaling pathways. JWA-increased GLT-1 expression was abolished by inhibitors of MEK and PI3K. Silencing CREB also abrogated JWA-increased GLT-1 expression and glutamate uptake. Additionally, JWA deficiency activated glial fibrillary acidic protein (GFAP), and increased the expression of STAT3. Similarly to the MPTP model, paraquat (PQ) exposure produced PD-like phenotypes in JWA CKO mice. Taken together, our findings provide novel insights into astrocytic JWA function in the pathogenesis of neurotoxin mouse models of PD.

Indexed as

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAmino Acid Transport System X-AGAnimalsAstrocytesCarrier ProteinsCyclic AMP Response Element-Binding ProteinDisease Models, AnimalDopamineDopaminergic NeuronsExcitatory Amino Acid Transporter 2Gene Knockout TechniquesGlial Fibrillary Acidic ProteinGlutamic AcidHeat-Shock ProteinsMaleMembrane Transport Proteins1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAmino Acid Transport System X-AGArl6ip5 protein, mouseCarrier ProteinsCreb1 protein, mouseCyclic AMP Response Element-Binding ProteinDopamineExcitatory Amino Acid Transporter 2Glial Fibrillary Acidic Proteinglial fibrillary astrocytic protein, mouseGlutamic AcidHeat-Shock ProteinsMembrane Transport ProteinsMitogen-Activated Protein KinasesNeurotoxinsParaquatPhosphatidylinositol 3-KinasesStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID29500411
PMCPMC5834463
OpenAlexW2792477001

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.