Transcriptome Analysis by RNA Sequencing of Mouse Embryonic Stem Cells Stocked on International Space Station for 1584 Days in Frozen State after Culture on the Ground

As a space project, in "Stem Cells" by the Japan Aerospace Exploration Agency (JAXA), frozen mouse ES cells were stored on the International Space Station (ISS) in the Minus Eighty Degree Laboratory Freezer for ISS (MELFI) for 1584 days. After taking these cells back to the ground, the cel...

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Veröffentlicht in:International journal of molecular sciences 2024-03, Vol.25 (6), p.3283
Hauptverfasser: Yoshida, Kayo, Hada, Megumi, Hayashi, Masami, Kizu, Akane, Kitada, Kohei, Eguchi-Kasai, Kiyomi, Kokubo, Toshiaki, Teramura, Takeshi, Hashizume Suzuki, Hiromi, Watanabe, Hitomi, Kondoh, Gen, Nagamatsu, Aiko, Saganti, Premkumar, Muratani, Masafumi, Cucinotta, Francis A, Morita, Takashi
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Sprache:eng
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Zusammenfassung:As a space project, in "Stem Cells" by the Japan Aerospace Exploration Agency (JAXA), frozen mouse ES cells were stored on the International Space Station (ISS) in the Minus Eighty Degree Laboratory Freezer for ISS (MELFI) for 1584 days. After taking these cells back to the ground, the cells were thawed and cultured, and their gene expressions were comprehensively analyzed using RNA sequencing in order to elucidate the early response of the cells to long-time exposure to space radiation consisting of various ionized particles. The comparisons of gene expression involved in double-stranded break (DSB) repair were examined. The expressions of most of the genes that were involved in homologous recombination (HR) and non-homologous end joining (NHEJ) were not significantly changed between the ISS-stocked cells and ground-stocked control cells. However, the transcription of Trp53inp1 (tumor protein 53 induced nuclear protein-1), Cdkn1a (p21), and Mdm2 genes increased in ISS-stocked cells as well as Fe ion-irradiated cells compared to control cells. This suggests that accumulated DNA damage caused by space radiation exposure would activate these genes, which are involved in cell cycle arrest for repair and apoptosis in a p53-dependent or -independent manner, in order to prevent cells with damaged genomes from proliferating and forming tumors.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms25063283