期刊文献+

60Coγ射线照射对血管内皮细胞生物学作用的影响

Effects of 60Coγ-ray irradiation on biological behaviors in human umbilical vein endothelial cells
下载PDF
导出
摘要 目的:观察^60 Coγ射线照射对血管内皮细胞生物学作用的影响。方法用不同剂量^60 Coγ射线照射人脐静脉血管内皮细胞( HUVEC),通过细胞生长曲线和克隆形成实验观察细胞增殖存活情况;流式细胞术检测照射后细胞周期的变化;中性单细胞凝胶电泳及蛋白印迹法( Western blot )观察细胞照射后DNA分子损伤及修复情况。结果^60 Coγ射线照射后, HUVEC细胞生长速度及增殖率降低,降低程度与照射剂量呈正相关;HUVEC细胞周期出现G2/M期阻滞;HUVEC细胞出现明显的DNA双链断裂,γH2AX和DNA-PKcs表达增加。结论^60 Coγ射线照射抑制血管内皮细胞增殖,导致G2/M期阻滞,促进DNA断裂,相关修复蛋白表达增加。 Objective To determine the effect of ^60 Coγ-ray irradiation on biological behaviors in cultured vascular endothelial cells in vitro.Methods Human umbilical vein endothelial cells ( HUVECs) were exposed to ^60 Coγ-ray irradiation at different doses .After irradiation , the proliferation of HUVECs was evaluated by cell growth curve and colony formation assay .Cell cycle was detected by flow cytometry.DNA damage and repair were analyzed by neutral single-cell gel electrophoresis , and the expression of related proteins was detected by Western blotting .Results After γ-ray irradiation , the proliferation of HUVECs was significantly inhibited in a dose-dependent manner.The cells were arrested at G 2/M stage after irradiation exposure .Obvious DNA double-strand breaks and enhanced expression of γH2AX and DNA-PKcs were observed in the HUVECs after irradiation .Conclusion ^60 Co γ-ray irradiation inhibits the proliferation of HUVECs, induces the cells arrested at G 2/M stage, promotes DNA break, and enhances the expression of repair-related proteins in endothelial cells .
出处 《中华老年多器官疾病杂志》 2016年第12期927-931,共5页 Chinese Journal of Multiple Organ Diseases in the Elderly
基金 国家自然科学基金项目(81102079) 中国博士后科学基金项目(201003776)~~
关键词 Γ射线 人脐静脉血管内皮细胞 细胞增殖 细胞周期 DNA损伤 gamma rays human umbilical vein endothelial cells cell proliferation cell cycle DNA injury
  • 相关文献

参考文献3

二级参考文献37

  • 1安静,黎鳌,杨宗城.胎儿脐静脉内皮细胞的培养[J].第三军医大学学报,1990,12(3):222-224. 被引量:51
  • 2胡舜英,邱乐,段海峰,王华,王荣亮,郭子宽,王立生,陈国伟.肝细胞生长因子在大鼠心肌细胞放射损伤中的抗凋亡作用[J].解放军医学杂志,2007,32(5):482-484. 被引量:3
  • 3[1]PASTWA E,BLASIAK J.Non-homologous DNA end joining[J].Acta Biochimica Polonica,2003,50 (4):891-908.
  • 4[2]MICHAEL R L,YUNMEI M,ULRICH P,et al.The mechanism vertebrate non-homologous DNA end joining and its role in V(D)J recombination[J].DNA Rep,2004,3(8):817-826.
  • 5[3]FISHEL R,WILSON T.Muts homologs in mammalian cells[J].Curr Op Gen,1997,Dev (7):105-113.
  • 6[4]O CONNOR T R,LAVAL F.Isolation and structure of a cDNA expressing a mammalian 3-methyladenime-DNA glycosylase[J].EMBO J,1990,9:3334-3337.
  • 7[5]CRAIG H,FREDERICK W A.The cellular response to general and proammed DNA double strand breaks[J].DNA Rep,2004,3:781-796.
  • 8[6]WETERINGS E,DIK C,GENT V.The mechanism of non-homologous end joining:A synopsis of synapsis[J].DNA Rep,2004,3:1425-1435.
  • 9[7]PIERCE A J,HU P,HAN M,et al.Ku DNA end-binding protein modulates homologous repair of double-strand breaks in mammalian cells[J].Genes Dev,2001,5:3237-3242.
  • 10[8]WALKER J R,CORPINA R A,GOLDBERG J,et al.Structure of the Ku heterodimer bound to DNA and its implications for double-strand break repair[J].Nature,2001,412:606-614.

共引文献12

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部