HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine >
Peer-reviewed Journal Articles, etc >

Analysis of the mechanism of radiation-induced upregulation of mitochondrial abundance in mouse fibroblasts.

Creative Commons License

Files in This Item:
final.pdf781.64 kBPDFView/Open
Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/66942

Title: Analysis of the mechanism of radiation-induced upregulation of mitochondrial abundance in mouse fibroblasts.
Authors: Yamamori, Tohru Browse this author →KAKEN DB
Sasagawa, Tomoya Browse this author
Ichii, Osamu Browse this author →KAKEN DB
Hiyoshi, Mie Browse this author
Bo, Tomoki Browse this author
Yasui, Hironobu Browse this author →KAKEN DB
Kon, Yasuhiro Browse this author →KAKEN DB
Inanami, Osamu Browse this author →KAKEN DB
Keywords: ionizing radiation
cellular radioresponse
mitochondria
mitochondrial biogenesis
cell cycle arrest
cellular senescence
Issue Date: 14-Dec-2016
Publisher: Oxford University Press
Journal Title: Journal of radiation research
Volume: 58
Issue: 3
Start Page: 292
End Page: 301
Publisher DOI: 10.1093/jrr/rrw113
PMID: 27974504
Abstract: Mitochondria strongly contribute to the maintenance of cellular integrity through various mechanisms, including oxidative adenosine triphosphate production and calcium homeostasis regulation. Therefore, proper regulation of the abundance, distribution and activity of mitochondria is crucial for the maintenance of cellular homeostasis. Previous studies have shown that ionizing radiation (IR) alters mitochondrial functions, suggesting that mitochondria are likely to be an important target of IR. Though IR reportedly influences cellular mitochondrial abundance, the mechanism remains largely unknown. In this study, we examined how IR influences mitochondrial abundance in mouse fibroblasts. When mouse NIH/3T3 cells were exposed to X-rays, a time-dependent increase was observed in mitochondrial DNA (mtDNA) and mitochondrial mass, indicating radiation-induced upregulation of mitochondrial abundance. Meanwhile, not only did we not observe a significant change in autophagic activity after irradiation, but in addition, IR hardly influenced the expression of two mitochondrial proteins, cytochrome c oxidase subunit IV and cytochrome c, or the mRNA expression of Polg, a component of DNA polymerase γ. We also observed that the expression of transcription factors involved in mitochondrial biogenesis was only marginally affected by IR. These data imply that radiation-induced upregulation of mitochondrial abundance is an event independent of macroautophagy and mitochondrial biogenesis. Furthermore, we found evidence that IR induced long-term cell cycle arrest and cellular senescence, indicating that these events are involved in regulating mitochondrial abundance. Considering the growing significance of mitochondria in cellular radioresponses, we believe the present study provides novel insights into understanding the effects of IR on mitochondria.
Rights: http://creativecommons.org/licenses/by-nc/4.0/
Type: article
URI: http://hdl.handle.net/2115/66942
Appears in Collections:獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 山盛 徹

Export metadata:

OAI-PMH ( junii2 , jpcoar )


 

Feedback - Hokkaido University