| 研究実績の概要 |
We explored the mechanisms of radiation induced chronic inflammation in human cells and in mouse models. We showed that vascular endothelial cells are sensitive to radiation exposure, and following low doses/dose rates exhibit growth arrest and robust Senescence Associated Secretory Phenotype. The significant increase in endothelial senescence leads to abnormal inflammatory phenotype and severe disruption of endothelial functions. Inhibition or knock-down of inflammatory regulators can abrogate senescence-associated inflammatory signaling, but do not affect entering senescence and cannot rescue the normal functioning of the endothelium. We also explored the cell composition of mouse aortas and the cytokine profile of irradiated LDR-/- mice to assess the in vivo relevance of these findings.
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