Evidence map›Paper›PMID 27469193›Full record

ArticleScientific reports2016

Far-infrared radiation protects viability in a cell model of Spinocerebellar Ataxia by preventing polyQ protein accumulation and improving mitochondrial function.

Jui-Chih Chang, Shey-Lin Wu, Fredrik Hoel, Yu-Shan Cheng, Ko-Hung Liu, Mingli Hsieh, August Hoel, Karl Johan Tronstad, Kuo-Chia Yan, Ching-Liang Hsieh and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-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

22 citing papers in PubMed, 39 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

14 authors at 5 institutions in 2 countries.

Jui-Chih ChangVascular and Genomic Center, Changhua Christian Hospital, Changhua 50094, Taiwan.
Shey-Lin WuDepartment of Neurology, Changhua Christian Hospital, Changhua 50094, Taiwan.
Fredrik HoelDepartment of Biomedicine, University of Bergen, 5020 Bergen, Norway.
Yu-Shan ChengDepartment of Neurology, Changhua Christian Hospital, Changhua 50094, Taiwan.
Ko-Hung LiuDepartment of Neurology, Changhua Christian Hospital, Changhua 50094, Taiwan.
Mingli HsiehDepartment of Life Science, Tunghai University, Taichung 40704, Taiwan.
August HoelDepartment of Biomedicine, University of Bergen, 5020 Bergen, Norway.
Karl Johan TronstadDepartment of Biomedicine, University of Bergen, 5020 Bergen, Norway.
Kuo-Chia YanDepartment of Dermatology, Changhua Christian Hospital, Changhua 50094, Taiwan.
Ching-Liang HsiehDepartment of Chinese Medicine, Obstetrics and Gynecology, Dermatology, and Urology, China Medical University Hospital, Taichung 40447, Taiwan.
Wei-Yong LinSchool of Chinese Medicine, Graduate Institute of Integrated Medicine, Research Center for Chinese Medicine and Acupuncture, China Medical University, Taichung 40447, Taiwan.
Shou-Jen KuoDepartment of Surgery, Changhua Christian Hospital, Changhua 50094, Taiwan.
Shih-Li SuDivision of Endocrinology and Metabolism, Department of Internal Medicine, Changhua Christian Hospital, Changhua 50094, Taiwan.
Chin-San LiuVascular and Genomic Center, Changhua Christian Hospital, Changhua 50094, Taiwan.
Changhua Christian Hospital · TWUniversity of Bergen · NOChina Medical University · TWChina Medical University Hospital · TWTunghai University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Far infrared radiation (FIR) is currently investigated as a potential therapeutic strategy in various diseases though the mechanism is unknown. Presently, we tested if FIR mediates beneficial effects in a cell model of the neurodegenerative disease spinocerebellar ataxia type 3 (SCA3). SCA3 is caused by a mutation leading to an abnormal polyglutamine expansion (PolyQ) in ataxin-3 protein. The consequent aggregation of mutant ataxin-3 results in disruption of vital cell functions. In this study, neuroblastoma cells (SK-N-SH) was transduced to express either non-pathogenic ataxin-3-26Q or pathogenic ataxin-3-78Q proteins. The cells expressing ataxin-3-78Q demonstrated decreased viability, and increased sensitivity to metabolic stress in the presence rotenone, an inhibitor of mitochondrial respiration. FIR exposure was found to protect against these effects. Moreover, FIR improved mitochondrial respiratory function, which was significantly compromised in ataxin-3-78Q and ataxin-3-26Q expressing cells. This was accompanied by decreased levels of mitochondrial fragmentation in FIR treated cells, as observed by fluorescence microscopy and protein expression analysis. Finally, the expression profile LC3-II, Beclin-1 and p62 suggested that FIR prevent the autophagy inhibiting effects observed in ataxin-3-78Q expressing cells. In summary, our results suggest that FIR have rescuing effects in cells expressing mutated pathogenic ataxin-3, through recovery of mitochondrial function and autophagy.

Indexed as

Infrared RaysModels, BiologicalAtaxin-3AutophagyCell Line, TumorCell RespirationCell SurvivalHumansMitochondriaMitochondrial DynamicsOxidative StressOxygen ConsumptionPeptidesSpinocerebellar AtaxiasAtaxin-3Peptidespolyglutamine

Identifiers

PMID27469193
PMCPMC4965738
OpenAlexW2490757276

What OpenQuestion holds

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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.