Evidence map›Paper›PMID 26415228›Full record

ArticleOncotarget2015

Low-dose ionizing radiation induces mitochondrial fusion and increases expression of mitochondrial complexes I and III in hippocampal neurons.

Ling Chien, Wun-Ke Chen, Szu-Ting Liu, Chuang-Rung Chang, Mou-Chieh Kao, Kuan-Wei Chen, Shih-Che Chiu, Ming-Ling Hsu, I-Chou Hsiang, Yu-Jen Chen and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 42 citations in OpenAlex.

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  5. Mitochondrial Signaling Pathways Associated with DNA Damage Responses.International journal of molecular sciences · 2023
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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

11 authors at 1 institution in 1 country.

Ling ChienInstitute of Molecular Medicine, National Tsing Hua University, Hsinchu, Taiwan, R.O.C.
Wun-Ke ChenDepartment of Radiation Oncology, MacKay Memorial Hospital, Taipei, Taiwan, R.O.C.
Szu-Ting LiuInstitute of Molecular Medicine, National Tsing Hua University, Hsinchu, Taiwan, R.O.C.
Chuang-Rung ChangDepartment of Medical Science, National Tsing Hua University, Hsinchu, Taiwan, R.O.C.
Mou-Chieh KaoInstitute of Molecular Medicine, National Tsing Hua University, Hsinchu, Taiwan, R.O.C.
Kuan-Wei ChenInstitute of Molecular Medicine, National Tsing Hua University, Hsinchu, Taiwan, R.O.C.
Shih-Che ChiuDepartment of Radiation Oncology, MacKay Memorial Hospital, Taipei, Taiwan, R.O.C.
Ming-Ling HsuDepartment of Radiation Oncology, MacKay Memorial Hospital, Taipei, Taiwan, R.O.C.
I-Chou HsiangDepartment of Radiation Oncology, MacKay Memorial Hospital, Taipei, Taiwan, R.O.C.
Yu-Jen ChenDepartment of Radiation Oncology, MacKay Memorial Hospital, Taipei, Taiwan, R.O.C.
Linyi ChenInstitute of Molecular Medicine, National Tsing Hua University, Hsinchu, Taiwan, R.O.C.
National Tsing Hua University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High energy ionizing radiation can cause DNA damage and cell death. During clinical radiation therapy, the radiation dose could range from 15 to 60 Gy depending on targets. While 2 Gy radiation has been shown to cause cancer cell death, studies also suggest a protective potential by low dose radiation. In this study, we examined the effect of 0.2-2 Gy radiation on hippocampal neurons. Low dose 0.2 Gy radiation treatment increased the levels of MTT. Since hippocampal neurons are post-mitotic, this result reveals a possibility that 0.2 Gy irradiation may increase mitochondrial activity to cope with stimuli. Maintaining neural plasticity is an energy-demanding process that requires high efficient mitochondrial function. We thus hypothesized that low dose radiation may regulate mitochondrial dynamics and function to ensure survival of neurons. Our results showed that five days after 0.2 Gy irradiation, no obvious changes on neuronal survival, neuronal synapses, membrane potential of mitochondria, reactive oxygen species levels, and mitochondrial DNA copy numbers. Interestingly, 0.2 Gy irradiation promoted the mitochondria fusion, resulting in part from the increased level of a mitochondrial fusion protein, Mfn2, and inhibition of Drp1 fission protein trafficking to the mitochondria. Accompanying with the increased mitochondrial fusion, the expressions of complexes I and III of the electron transport chain were also increased. These findings suggest that, hippocampal neurons undergo increased mitochondrial fusion to modulate cellular activity as an adaptive mechanism in response to low dose radiation.

Indexed as

Radiation, IonizingAnimalsCell PlasticityCells, CulturedCell SurvivalDNA, MitochondrialDynaminsElectron Transport Complex IElectron Transport Complex IIIGene DosageGTP PhosphohydrolasesHippocampusMembrane Potential, MitochondrialMembrane ProteinsMitochondriaMitochondrial DynamicsDNA, MitochondrialDnm1l protein, ratDynaminsElectron Transport Complex IElectron Transport Complex IIIGTP PhosphohydrolasesMembrane ProteinsMfn2 protein, ratMitochondrial ProteinsReactive Oxygen Specieshippocampal neuronslow dose radiationmitochondrial fusionPathology Sectionradiation therapy

Identifiers

PMID26415228
PMCPMC4741557
OpenAlexW1948675936

What Socratic 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 Socratic graph.