>
网站首页期刊介绍通知公告编 委 会投稿须知电子期刊广告合作联系我们
最新消息:
离子辐射通过caspase途径而非p53途径诱导Jurkat细胞凋亡
作者:刘家浩 唐洪丽 阮为勇 王伟 唐月华 
单位:东南大学附属中大医院儿科,江苏,南京,210009
关键词:半胱氨酸天冬氨酸蛋白酶 基因 p53 细胞凋亡/辐射效应 Jurkat细胞 RNA 信使 
分类号:R-33, Q345.2, R733.705
出版年·卷·期(页码):2005·24·第四期(213-217)
摘要:

目的:研究离子辐射诱导Jurkat细胞凋亡的动态趋势及其机制.方法:分别以5、10、20Gy的辐射量照射Jurkat细胞,其中一份样本在照射前加入zVAD.fmk,在照射后培养6、12、24、36和48 h收获细胞,应用AnV/PI双染和呈现sub-G1峰技术,在流式细胞仪上定量测定凋亡细胞.采用Western Blot技术检测p53蛋白的表达.结果:细胞受照射后,凋亡细胞数随培养时间的延长和辐射量的加大而增加.在6 h,只有20Gy才诱导细胞显著凋亡(P<0.005),5Gy的照射要到24h才出现明显的凋亡(P<0.05).在48h,20Gy照射诱导的凋亡细胞数是所有时间点和剂量强度中最高的(P<0.001).加有zVAD.fmk的细胞,尽管都是10Gy照射,比未加zVAD.fmk的细胞表现出凋亡细胞明显减少(P<0.005),但与未加zVAD.fmk、照射量是5Gy的细胞相比,凋亡细胞数仍显著增加(P<0.005).Jurkat细胞在照射前后都没有p53表达.结论:离子辐射诱导细胞凋亡呈现出时间和剂量效应关系;capase抑制剂zVAD.fmk部分抑制离子辐射诱导细胞凋亡;离子辐射诱导细胞凋亡的机制独立于肿瘤抑制基因p53,caspase可能在其中起重要作用.

参考文献:

[1] Verheij M, BARTELINK H. Radiation-induced apoptosis. 2000. doi:10.1007/s004410000188
[2] SHEARD M A. Ionizing radiation as a response-enhancing agent for CD95-mediated apoptosis. 2001(4). doi:10.1002/ijc.1020
[3] Zhou L, YUAN R, SERGGIO L. Molecular mechanisms of irradiation- induced apoptosis. 2003. doi:10.2741/927
[4] Ferlini C, D'AMLIO R, SCAMBIA G. Apoptosis induced by ionizing radiation. The biological basis and radiosensitivity, 2002
[5] Shinomiya N. New concepts in radiation- induced apoptosis:"premitotic apoptosis" and "postmitotic apoptosis", 2001
[6] MIP ZAIE-JONIANI H, ERIKSSEON D, SHEIKHOLVAEZIN A. Apoptosis induced by low-dose and low-dose-rate radiation. 2002(4 suppl). doi:10.1002/cncr.10287
[7] ISRAELS L, ISRAELS E D. Apoptosis. 1999(5). doi:10.1002/stem.170306
[8] PAN L F R, PENNINGS A H M, VIERWINDEN G. The dynamic process of apoptosis analyzed by flow cytometry using anneixn-V/propidium iodine and a modified in situ end labeling technique. 2002
[9] BOESEN-de-COCK J G, TEPPER A D, de VRIES E. Common regulation of apoptosis signaling induced by CD95 and the DNA-damage stimuli etoposide and γ-radiation downstream from caspase-8 activation. 1999
[10] Nicholson D W. Caspase structure, proteolytic substrates, and function during apoptotic cell death. 1999(6). doi:10.1038/sj.cdd.4400598
[11] PHILCHENKOW A, ZAVELEVICH M, KROCZAK T J. Caspases and cancer:mechanisms of inactivation and new treatment modalities, 2004(2)
[12] PERRY M E. Mdm2 in the response to rndiation. 2004
[13] FEI P, EL-DEIR W S. p53 and radiation responses. 2003(37). doi:10.1038/sj.onc.1206677
[14] Hasegawa M, MITSUHASHI N, YAMAKAWA M. p53protein expression and radiation-induced apoptosis in human tumors transplanted to nude mice, 1997
[15] Shimada H, MATSUBARA H, OCHIAI T. p53 Gene therapy for esophageal cancer. 2002(z14)
[16] Obata A, EURA M, SASAKI J. Clinical significance of p53functional loss in squamous cell carcinoma of the oropharynx. 2000(2). doi:10.1002/(SICI)1097-0215(20000320)89:2&lt, 187::AID-IJC14&gt, 3.0.CO, 2-V  

服务与反馈:
文章下载】【发表评论】【查看评论】【加入收藏
提示:您还未登录,请登录!点此登录
您是第 412653 位访问者


copyright ©《东南大学学报(医学版)》编辑部
联系电话:025-83272481 83272483
电子邮件:
bjb@pub.seu.edu.cn

苏ICP备09058364