Low-dose of Ionizing Radiation Enhances Cell Proliferation Via Transient ERK1/2 and p38 Activation in Normal Human Lung Fibroblasts
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- KIM Cha Soon
- Radiation Health Research Institute, Korea Hydro & Nuclear Power Co., LTD School of Life Sciences & Biotechnology, Korea University
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- KIM Jin-Mo
- Radiation Health Research Institute, Korea Hydro & Nuclear Power Co., LTD Inha University College of Medicine, Department of Physiology
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- NAM Seon Young
- Radiation Health Research Institute, Korea Hydro & Nuclear Power Co., LTD
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- YANG Kwang Hee
- Radiation Health Research Institute, Korea Hydro & Nuclear Power Co., LTD
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- JEONG Meeseon
- Radiation Health Research Institute, Korea Hydro & Nuclear Power Co., LTD
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- KIM Hee Sun
- Radiation Health Research Institute, Korea Hydro & Nuclear Power Co., LTD
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- LIM Young-Khi
- Radiation Health Research Institute, Korea Hydro & Nuclear Power Co., LTD
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- KIM Chong Soon
- Radiation Health Research Institute, Korea Hydro & Nuclear Power Co., LTD
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- JIN Young-Woo
- Radiation Health Research Institute, Korea Hydro & Nuclear Power Co., LTD
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- KIM Joon
- School of Life Sciences & Biotechnology, Korea University
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This study shows the human cellular responses and the mechanism of low-dose ionizing radiation in CCD 18 Lu cells, which are derived from normal human lung fibroblasts. Cell proliferation and viability assay were measured for the cells following γ-irradiation using trypan blue, BrdU incorporation, and Wst-1 assay. We also examined genotoxicity using a micronuclei formation assay. The activation of the MAPKs pathway was determined by Western blot analysis, and the siRNA system was used to inhibit the expression of ERK1/2 and p38. We found that 0.05 Gy of ionizing radiation stimulated cell proliferation and did not change Micronuclei frequencies. In addition, 0.05 Gy of ionizing radiation activated ERK1/2 and p38, but did not activate JNK1/2 in cells. A specific ERK1/2 inhibitor, U0126, decreased the phosphorylation of ERK1/2 proteins induced by 0.05 Gy of ionizing radiation, and a similar suppressive effect was observed with a p38 inhibitor, PD169316. Suppression of ERK1/2 and p38 phosphorylation with these inhibitors decreased cell proliferation, which was stimulated by 0.05 Gy of ionizing radiation. Furthermore, downregulation of ERK1/2 and p38 expression using siRNA blocked the cell proliferation that had been increased by 0.05 Gy of ionizing radiation. These results suggest that 0.05 Gy of ionizing radiation enhances cell proliferation through the activation of ERK1/2 and p38 in normal human lung fibroblasts.<br>
収録刊行物
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- Journal of Radiation Research
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Journal of Radiation Research 48 (5), 407-415, 2007
Journal of Radiation Research 編集委員会
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詳細情報 詳細情報について
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- CRID
- 1390001205215210624
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- NII論文ID
- 110006388623
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- NII書誌ID
- AA00705792
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- ISSN
- 13499157
- 04493060
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- NDL書誌ID
- 8911823
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- NDL-Digital
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可