Biological Effects of Space Radiation and Microgravity on Mammalian Cells (NeuroRad) - 09.17.14

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Biological Effects of Space Radiation and Microgravity on Mammalian Cells (NeuroRad) studies the effects of space radiation on the human neuroblastoma cell (nerve cell containing a tumor) line in microgravity.

Science Results for Everyone

Space travel is rough on human cells.  Studying human nerve cells with tumors, and changes in their genetic materials, show that short- and long-term cultures of these cells on the space station grow faster and generate more reactive oxygen species, along with increased heat shock proteins and antioxidant enzymes than those cultured on Earth, meaning that toxic stress occurs in the microgravity cells.  Results could advance new treatments and preventative measures for the effects of radiation on humans in space and for related diseases and aging on Earth.

The following content was provided by Hideyuki J. Majima, Ph.D., and is maintained in a database by the ISS Program Science Office.
Information provided courtesy of the Japan Aerospace and Exploration Agency (JAXA).

Experiment Details


Principal Investigator(s)

  • Hideyuki J. Majima, Ph.D., Kagoshima University, Kagoshima, Japan

  • Co-Investigator(s)/Collaborator(s)
  • Shigeaki Suenaga, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan
  • Misato Oki, Kagoshima University, Japan
  • Kenichiro Matsumoto, National Institute of Radiological Sciences, Chiba, Japan
  • Kazunobu Fujitaka, NIRS, Japan
  • Masaki Kameyama, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan
  • Yoichiro Iwashita, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan
  • Kazuhiko Saigo, Kagoshima University, Japan
  • Ikuo Nakanishi, National Institute of Radiological Sciences, Chiba, Japan
  • Noriaki Ishioka, Japan Aerospace and Exploration Agency, Tsukuba City, Japan
  • Hiroko P. Indo, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan
  • Hiromi Suzuki, Japan Space Forum, Chiyoda-ku Ootemachi, Japan
  • Toru Shimazu, Japan Space Forum, Tokyo, Japan
  • Sachiko Yano, JAXA Space Environment Utilization Center, Ibaraki 305-8505, Japan
  • Fumiaki Tanigaki, JAXA, Ibaraki, Japan
  • Daisuke Masuda, Japan Manned Space System , Tsuchiura, Japan

  • Developer(s)
    Information Pending
    Sponsoring Space Agency
    Japan Aerospace Exploration Agency (JAXA)

    Sponsoring Organization
    Information Pending

    Research Benefits
    Information Pending

    ISS Expedition Duration
    March 2010 - September 2010

    Expeditions Assigned

    Previous ISS Missions
    NeuroRad was first operated on ISS Expedition 19/20.

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    Experiment Description

    Research Overview

    • NeuroRad will investigate the biological effects of space radiation on mammalian nerve cells using SK-N-SH (human neuroblastoma cell line).

    • NeuroRad will evaluate the risk factors of long-term space flight by investigating the ability to recover from radiation damage aquired in microgravity. NeuroRad will also evaluate the effects of radiation accumulation as a result of long-term space flight missions.

    • NeuroRad will focus on changes in the mitochondria-related gene expression, since the mitochondria is well known for having a crucial role in apotosis (programmed cell death).

    • After recovery, the effects of radiation in microgravity will be comprehensively analyzed using the following techniques: nuclear DNA microaray, western blotting, and mutation assays.

    Information Pending

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    Space Applications
    Information Pending

    Earth Applications
    Radiation effects are critical for biological creatures. The data collected during this investigation may lead a greater understanding of how the radiation defense system is affected by different factors from space radiation and microgravity environment. The data could be applied to develop new treatments and preventative measures for the effects of radiation, and to further investigate the effects of human long-duration stays in space.

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    Operational Requirements
    Information Pending

    Operational Protocols
    Information Pending

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    Results/More Information

     Researchers investigated the transcription factors that regulate Cbl-b expression using rat L6 myoblasts and differentiated myotubes. The biological relevance of Cbl-b expression as a sensor of unloading is strengthened by the findings that both oxidative stress and 3-D-clinorotation induced Cbl-b expression in L6 myoblasts and myotubes. These findings suggest that increased levels of ROS link mechanical stress to downstream signaling pathways. In the present study, we observed that H2O2 treatment promoted the binding of Egr to the 5'-franking region of Cbl-b gene. Moreover, 3-D-clinorotation and H2O2 each induced the expression of Cbl-b in a manner accompanied by the early expression of Egrs 1-3. This is consistent with the findings of another laboratory using Egr-2 or Egr-3 knockout mice. The results obtained in Egr knockdown studies (siRNA) confirm that Egr transcription factors play a major role in 3-D-clinorotation-mediated Cbl-b induction. Together, these data uncover the molecular mechanism through which mechanical unloading is transduced into biochemical signaling in skeletal muscle.        Several lines of evidence in diverse cell types point to the involvement of Egr transcription factors in the response to mechanical stress. Egr expression induced by 3-D-clinorotation occurs within 90 minutes of stimulation, indicating that the Egr genes are in close temporal proximity to the mechanical stress “receptor.” Consistent with the role of oxidants as the second messengers of Egr activation and downstream unloading responses, the ERK1/2 pathway, a common target of oxidative signaling, was activated by 3-D-clinorotation and H2O2. Together, these results are consistent with the findings of other laboratories; they showed that immobilization or tail suspension increased oxidative stress-dependent signaling in rat skeletal muscles. Recent studies have identified several signaling molecules, such as ASK1, that mediate oxidative stress-dependent activation of MAPK signaling. An important area for further investigation will be to identify the molecules that regulate ROS production in distinct cellular compartments (plasma membrane, mitochondria) in response to unloading. It is anticipated that these molecules may be the direct receptors/sensors for unloading stress. This hypothesis is supported by previous finding that the disrupted expression of cytoskeletal genes, especially mitochondria-anchoring protein genes, is associated with large imbalances in the expression of genes encoding diverse members of the electron transport system in the mitochondria of space-flown skeletal muscle. 


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    Results Publications

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    Ground Based Results Publications

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    ISS Patents

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    Related Publications

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    Related Websites

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