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Macrophage-Mediated Bystander Effects after Different Irradiations through a p53-dependent Pathway
Jiamei Fu1,2, Lin Zhu2, Wenzhi Tu2
1Department of Radiation Oncology, Shanghai Pulmonary Hospital, Tongji University, School of Medicine, Shanghai, 200433, China.
Radiation Research
|December 17, 2019
Summary
Bystander cells outside radiation fields can experience damage, especially when macrophages are involved. Radiation type and the p53 pathway in irradiated cells influence this cell damage, potentially causing lymphocytopenia.
Area of Science:
- Radiobiology
- Cellular and Molecular Medicine
- Radiation Oncology
Background:
- Bystander effects occur outside the direct radiation field, posing risks for hematological toxicity.
- Understanding intercellular communication and signaling pathways is crucial for managing radiation side effects.
Purpose of the Study:
- To investigate bystander effects and their hematological toxicity mechanisms.
- To explore intercellular communication between irradiated and bystander cells, including the role of macrophages.
Main Methods:
- Utilized an in vitro multicellular co-culture system with A549, Beas-2B, TK6, and U937 cells.
- Investigated effects of gamma rays and carbon ion irradiation on cell proliferation and viability.
- Examined the involvement of the p53-apoptosis pathway and macrophage mediation.
Main Results:
- Bystander TK6 cell proliferation was inhibited by gamma-irradiated A549 cells, an effect amplified by macrophages.
- Carbon ion irradiation caused more severe bystander cell injury than gamma rays.
- p53 pathway activation in irradiated cells was linked to bystander damage, which was alleviated by p53 inhibition.
Conclusions:
- Bystander lymphoblast damage is induced by different radiation types (gamma rays, carbon ions) and modulated by macrophages.
- The p53-apoptosis pathway in irradiated cells is a key mechanism underlying bystander effects.
- These findings suggest bystander and macrophage-mediated effects contribute to radiation-induced lymphocytopenia.
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