| SUN Hua-li,DUAN Wei-ming,SHAO Yan-yan,XIAO Hai-nan,ZHOU Xin-wen.Delayed K562 cell apoptosis promoted by cleaved LyGDI after 60 Co γ-rays irradiation[J].Chinese Journal of Radiological Medicine and Protection,2010,30(6):643-646 |
| Delayed K562 cell apoptosis promoted by cleaved LyGDI after 60 Co γ-rays irradiation |
| Received:July 13, 2010 |
| DOI： |
| KeyWords:60 Co γ-rays LyGDI Rac1 Apoptosis |
| FundProject:国家自然科学基金(30570548) |
| Author Name | Affiliation | E-mail | | SUN Hua-li | School of Radiation Medicine and Public Health, Soochow University, Suzhou 215123, China | | | DUAN Wei-ming | 苏州大学附属第一医院 肿瘤科 | | | SHAO Yan-yan | School of Radiation Medicine and Public Health, Soochow University, Suzhou 215123, China | | | XIAO Hai-nan | School of Radiation Medicine and Public Health, Soochow University, Suzhou 215123, China | | | ZHOU Xin-wen | School of Radiation Medicine and Public Health, Soochow University, Suzhou 215123, China | xwzhou@suda.edu.cn |
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| Abstract:: |
| Objective To elucidate the function and regulatory mechanism of LyGDI involved delayed cell death in the human K562 cells and HL-60 cells induced by 60Co γ-rays. Methods Erythrosine B cells staining was used to count the apoptosis rate. PI staining and flow cytometry were applied to check the cell cycle. The expression of LYGDI and Rac1 was resolved by Western blot by using monoclonal antibody of LyGDI and Rac1.The distribution of Rac1 protein in cells was observed with immunofluorescence by using the confocal microscope. Results The K562 cells showed G2/M phase arrest and the percent age was 71.3%. The apoptosis rate was very low at early post-irradiation stage in the K562 cells.The apoptosis rate was 14% in the K562 cells at 24 h post-irradiation with 8 Gy of γ-rays, and delayed cell apoptosis was present. LyGDI was cleaved in the K562 cells irradiated by 4 Gy 60 Co γ-rays after 24 hours post-irradiation. The expression of Rac1 protein was not altered at all, but the distribution was changed in the irradiated cells while the Rac1 protein moved to cell membrane and a little in cell nucleus. The Rac1 was activated with the losing the binding affinity with the LyGDI.Conclusion LyGDI could promote the delayed cell apoptosis, which is through the activation of the Rac1. |
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