Delayed K562 cell apoptosis promoted by cleaved LyGDI after 60Co γ-rays irradiation
10.3760/cma.j.issn.0254-5098.2010.06.004
- VernacularTitle:60 Coγ射线辐射致LyGDI断裂对K562细胞的延迟性凋亡作用
- Author:
Huali SUN
;
Weiming DUAN
;
Yanyan SHAO
;
Hainan XIAO
;
Xinwen ZHOU
- Publication Type:Journal Article
- Keywords:
60 Co γ-rays;
LyGDI;
Rac1;
Apoptosis
- From:
Chinese Journal of Radiological Medicine and Protection
2010;30(6):643-646
- CountryChina
- Language:Chinese
-
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 Racl. The distribution of Racl 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 Racl protein was not altered at all, but the distribution was changed in the irradiated cells while the Racl protein moved to cell membrane and a little in cell nucleus. The Racl 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.
