许志祥,张学光,强亦忠,徐颖,施勤,朱剑昆,丁天.重组人Flt3配体对微血管内皮细胞的抗辐射作用研究[J].中华放射医学与防护杂志,2001,21(4):286-289
重组人Flt3配体对微血管内皮细胞的抗辐射作用研究
The influence of Flt3 ligand on proliferation of irradiated microvascular endothelial cells
投稿时间:2000-11-21  
DOI:
中文关键词:  Flt3配体  造血微环境  微血管内皮细胞(ECV)  辐射  增殖  凋亡
英文关键词:Flt3 ligand  Hematopoietic micro-environment  Microvascular endothelial cell(ECVs)  Irradiation  Proliferation  Apoptosis
基金项目:国防科工委国防预研基金资助项目(Y5573162);国际原子能机构(IAEA)基金资助项目(CRP9025)
作者单位
许志祥 215007 江苏, 苏州大学核医学生物技术重点实验室、医学生物技术研究所 
张学光 215007 江苏, 苏州大学核医学生物技术重点实验室、医学生物技术研究所 
强亦忠 215007 江苏, 苏州大学核医学生物技术重点实验室、医学生物技术研究所 
徐颖 215007 江苏, 苏州大学核医学生物技术重点实验室、医学生物技术研究所 
施勤 215007 江苏, 苏州大学核医学生物技术重点实验室、医学生物技术研究所 
朱剑昆 215007 江苏, 苏州大学核医学生物技术重点实验室、医学生物技术研究所 
丁天 上海复旦大学生化系 
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中文摘要:
      目的 研究Flt3配体 (FL)对人微血管内皮细胞系细胞 (ECV)的抗辐射作用及其可能的作用机理.方法 用流式细胞仪分析ECV表面Flt3受体的表达;用MTT法观察FL对受照射ECV增殖的影响;用Annexin V-PI方法测定细胞凋亡,用RT-PCR方法分析细胞凋亡基因bax和Bcl-2的改变.结果 ECV表达Flt3受体,FL能激发ECV增殖,ECV经 15Gy的照射后,FL能有效地拮抗照射对ECV增殖的抑制作用;同时照射后ECV的bax基因表达增加,bcl-2基因表达轻度降低.FL通过抑制bax基因的表达,降低辐射引起的ECV细胞凋亡.结论 FL通过抑制细胞凋亡,减轻辐射引起的ECV的损伤,可能在辐射损伤患者造血微环境的保护中具有应用价值.
英文摘要:
      Objective To investigate the influence of FL on proliferation of irradiated microvascular endothelial cells (ECVs),and possible mechanism of FL in radiation protection of ECVs. Methods The ECVs were screened for Flt3 receptor expression by flow cytometric analysis.The proliferation of ECVs stimulated by FL was measured by the microculture tetrazolium assay (MTT).The apoptosis of ECVs caused by irradiation was measured with Annexin V PI.Two apoptosis related genes,Bcl-XL and Bax,were also analyzed by RT-PCR. Results Flt3 receptors were expressed on the surface of ECVs.FL stimulated the proliferation of ECVs at very low concentrations (0.5-15 ng/ml) with the maximum stimulation at 15 ng/ml.A significant increase in Bax activity and a decrease in Bcl XL activity were seen at 24 h and 48 h post-irradiation,respectivety. When the culture medium with FL was added 2 h before or immediately after irradiation,the expression of Bax fell sharply at 24 h and 48 h post-irradiation.The change in Bcl-XL activity was not so marked and a mild increase in Bcl-XL expression was seen only at 48 h post-irradiation.FL inhibited the apoptosis of ECVs caused by irradiation and stimulated the proliferation of irradiated ECVs. Conclusion FL down-regulates the expression of Bax in irradiated ECVs,and inhibits the apoptosis of the ECVs.Thus,FL may find a use in radio-protection of hematopoietic cells via protection of the microvascular endothelial cells in the bone marrow microenvironment.
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