Evidence map›Paper›PMID 26156288›Full record

ArticleMolecular neurobiology2016

The Neuroprotective Effect of Erythropoietin on Rotenone-Induced Neurotoxicity in SH-SY5Y Cells Through the Induction of Autophagy.

Wooyoung Jang, Hee Ju Kim, Huan Li, Kwang Deog Jo, Moon Kyu Lee, Hyun Ok Yang

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 94 citations in OpenAlex.

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  17. Artemisinin attenuated oxidative stress and apoptosis by inhibiting autophagy in MPPJournal of biological research (Thessalonike, Greece) · 2021
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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

6 authors at 4 institutions in 1 country.

Wooyoung JangDepartment of Neurology, Gangneung Asan Hospital, University of Ulsan College of Medicine, Bangdong-ri, Sacheon-myeon, Gangneung, Gangwon-do, 210-711, Republic of Korea. neveu@gnah.co.kr.
Hee Ju KimNatural Products Research Center, Korea Institute of Science and Technology, 679 Saimdang-ro, Gangneung, 210-340, Republic of Korea.
Huan LiNatural Products Research Center, Korea Institute of Science and Technology, 679 Saimdang-ro, Gangneung, 210-340, Republic of Korea.
Kwang Deog JoDepartment of Neurology, Gangneung Asan Hospital, University of Ulsan College of Medicine, Bangdong-ri, Sacheon-myeon, Gangneung, Gangwon-do, 210-711, Republic of Korea.
Moon Kyu LeeDepartment of Neurology, Gangneung Asan Hospital, University of Ulsan College of Medicine, Bangdong-ri, Sacheon-myeon, Gangneung, Gangwon-do, 210-711, Republic of Korea.
Hyun Ok YangNatural Products Research Center, Korea Institute of Science and Technology, 679 Saimdang-ro, Gangneung, 210-340, Republic of Korea. hoyang@kist.re.kr.
Korea Institute of Science and Technology · KRUniversity of Ulsan · KRGangneung Asan Hospital · KRUlsan College · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Currently, the autophagy pathway is thought to be important for the pathogenesis of Parkinson's disease (PD), and the modulation of autophagy may be a novel strategy for the treatment of this disease. Erythropoietin (EPO) has been reported to have neuroprotective effects through anti-oxidative, anti-apoptotic, and anti-inflammatory mechanisms, and it has also been shown to modulate autophagy signaling in an oxygen toxicity model. Therefore, we investigated the effects of EPO on autophagy markers and evaluated its neuroprotective effect on rotenone-induced neurotoxicity. We adapted the rotenone-induced neurotoxicity model to SH-SY5Y cells as an in vitro model of PD. We measured cell viability using MTT and annexin V/propidium iodide assays and measured intracellular levels of reactive oxygen species. Immunofluorescence analysis was performed to measure the expression of LC3 and α-synuclein. Intracellular signaling proteins associated with autophagy were examined by immunoblot analysis. EPO mono-treatment increased the levels of mammalian target of rapamycin (mTOR)-independent/upstream autophagy markers, including Beclin-1, AMPK, and ULK-1. Rotenone treatment of SH-SY5Y cells reduced their viability, increased reactive oxygen species levels, and induced apoptosis and α-synuclein expression, and simultaneous exposure to EPO significantly reduced these effects. Rotenone enhanced mTOR expression and suppressed Beclin-1 expression, indicating suppression of the autophagy system. However, combined treatment with EPO restored Beclin-1 expression and decreased mTOR expression. EPO protects against rotenone-induced neurotoxicity in SH-SY5Y cells by enhancing autophagy-related signaling pathways. The experimental evidence for the EPO-induced neuroprotection against rotenone-induced dopaminergic neurotoxicity may significantly impact the development of future PD treatment strategies.

Indexed as

alpha-SynucleinApoptosisAutophagyCell DeathCell Line, TumorErythropoietinHumansIntracellular SpaceMicrotubule-Associated ProteinsNeuroprotective AgentsNeurotoxinsReactive Oxygen SpeciesRotenoneSignal Transductionalpha-SynucleinErythropoietinMAP1LC3A protein, humanMicrotubule-Associated ProteinsNeuroprotective AgentsNeurotoxinsReactive Oxygen SpeciesRotenoneAutophagyErythropoietinNeuroprotectionParkinson’s disease

Identifiers

PMID26156288
OpenAlexW771094432

What OpenQuestion holds

Textmetadata
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.