Evidence map›Paper›PMID 26085927›Full record

ArticleTranslational neurodegeneration2015

Wnt3a protects SH-SY5Y cells against 6-hydroxydopamine toxicity by restoration of mitochondria function.

Lei Wei, Li Ding, Ming-Shu Mo, Ming Lei, Limin Zhang, Kang Chen, Pingyi Xu

Open access · goldAbstract read
In one paragraph

Article in Translational neurodegeneration, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
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  13. Modification of Wnt signaling pathway on paraquat-induced inhibition of neural progenitor cell proliferation.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2018
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  20. Regeneration in the nervous system with erythropoietin.Frontiers in bioscience (Landmark edition) · 2016
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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

7 authors at 4 institutions in 1 country.

Lei WeiDepartment of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630 China ; Department of Neurology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080 China.
Li DingDepartment of pathology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080 China.
Ming-Shu MoDepartment of Neurology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080 China.
Ming LeiDepartment of Neurology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080 China.
Limin ZhangDepartment of Neurology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080 China.
Kang ChenDivision of Clinical Laboratory, Zhongshan Hospital of Sun Yat-sen University, Zhongshan, 528403 China.
Pingyi XuDepartment of Neurology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080 China ; Department of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120 China.
Sun Yat-sen University · CNFirst Affiliated Hospital of Guangzhou Medical University · CNThe First Affiliated Hospital, Sun Yat-sen University · CNThird Affiliated Hospital of Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWnt/β-catenin signal has been reported to exert cytoprotective effects in cellular models of several diseases, including Parkinson's disease (PD). This study aimed to investigate the neuroprotective effects of actived Wnt/β-catenin signal by Wnt3a on SH-SY5Y cells treated with 6-hydroxydopamine (6-OHDA).

methodsWnt3a-conditioned medium (Wnt3a-CM) was used to intervene dopaminegic SH-SY5Y cells treated with 6-OHDA. Cell toxicity was determined by cell viability and lactate dehydrogenase leakage (LDH) assay. The mitochondria function was measured by the mitochondrial membrane potential, while oxidative stress was monitored with intracellular reactive oxygen species (ROS). Western blot analysis was used to detect the expression of GSK3β, β-catenin as well as Akt.

resultsOur results showed that 100 μM 6-OHDA treated for 24 h significantly decreased cell viability and mitochondrial transmembrane potential, reduced the level of β-catenin and p-Akt, increased LDH leakage, ROS production and the ratio of p-GSK3β (Tyr216) to p-GSK3β (Ser9). However, Wnt3a-conditioned medium reversing SH-SY5Y cells against 6-OHDA-induced neurotoxicity by reversing these changes.

conclusionsActivating of Wnt/β-catenin pathway by Wnt3a-CM attenuated 6-OHDA-induced neurotoxicity significantly, which related to the inhibition of oxidative stress and maintenance of normal mitochondrial function.

Indexed as

6-OHDAMitochondria functionParkinson’s diseaseWnt3a

Identifiers

PMID26085927
PMCPMC4470059
OpenAlexW2120177259

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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.