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Abstract
Purpose
Astronauts exhibit neurological dysfunction during long-duration spaceflight, and the specific mechanisms may be closely related to the cumulative effects of these neurological injuries in the space radiation environment. Here, we investigated the interaction between astrocytes and neuronal cells exposed to simulated space radiation.
Materials and methods
we selected human astrocytes (U87 MG) and neuronal cells (SH-SY5Y) to establish an experimental model to explore the interaction between astrocytes and neuronal cells in the CNS under simulated space radiation environment and the role of exosomes in the interactions.
Results
We found that γ-ray caused oxidative and inflammatory damage in human U87 MG and SH-SY5Y. The results of the conditioned medium transfer experiments showed that astrocytes exhibited a protective effect on neuronal cells, and neuronal cells influenced the activation of astrocytes in oxidative and inflammatory injury of CNS. We demonstrated that the number and size distribution of exosomes derived from U87 MG and SH-SY5Y cells were changed in response to H2O2, TNF-α or γ-ray treatment. Furthermore, we found that exosome derived from treated nerve cells influenced the cell viability and gene expression of untreated nerve cells, and the effect of exosomes was partly consistent with that of the conditioned medium.
Conclusion
Our findings demonstrated that astrocytes showed a protective effect on neuronal cells, and neuronal cells influenced the activation of astrocytes in oxidative and inflammatory damage of CNS induced by simulated space radiation. Exosomes played an essential role in the interaction between astrocytes and neuronal cells exposed to simulated space radiation.
Acknowledgments
We thank the Biological and Medical Engineering Core Facilities of the Beijing Institute of Technology and Beijing Key Laboratory for Separation and Analysis in Biomedicine and Pharmaceuticals for supporting experimental equipment.
Disclosure statement
The authors declare no conflicts of interest.
Additional information
Funding
Notes on contributors
Mengjin Liu
Mengjin Liu, MD, her research field is Neurobiology. In the present study she performed investigation, data analysis and original draft preparation.
Yu Lan
Yu Lan, MD, his research field is Neurobiology. In the present study he performed investigation and data analysis.
Yuhan Qin
Yuhan Qin, MD, his research field is Neurobiology. In the present study he performed validation.
Yanan Gao
Yanan Gao, PhD, her research field is Neurobiology. In the present study she performed validation.
Yulin Deng
Yulin Deng, Professor of School of Life Sciences, Beijing Institute of Technology; Member of the International Academy of Astronautics, President of the Life Sciences Committee of the International Academy of Astronautics. In the present study he performed manuscript review and editing.
Nuomin Li
Nuomin Li, PhD, associate researcher of the School of Medical Technology, Beijing Institute of Technology. Dr. Li engaged in the research on the molecular mechanism of neurodegenerative diseases. She has published over 15 papers in international journals. In the present study she performed manuscript review and editing.
Chen Zhang
Chen Zhang, PhD, graduated from Peking Union Medical College, majoring in biochemistry and molecular biology. His research interests include the role of environmental pollutants in inducing cardiotoxicity and its molecular mechanism. In the present study he performed design of experimental scheme, data analysis and original draft preparation.
Hong Ma
Hong Ma, Professor of School of Life Sciences, Beijing Institute of Technology. Her research interests are in space biology and medical engineering. In the present study she performed design of experimental scheme, review and editing the manuscript.