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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Radiat+Res
2017 ; 58
(3
): 292-301
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Analysis of the mechanism of radiation-induced upregulation of mitochondrial
abundance in mouse fibroblasts
#MMPMID27974504
Yamamori T
; Sasagawa T
; Ichii O
; Hiyoshi M
; Bo T
; Yasui H
; Kon Y
; Inanami O
J Radiat Res
2017[May]; 58
(3
): 292-301
PMID27974504
show ga
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 ?. 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.
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