Analysis of the intracellular regulatory mechanism of bcl-2 related apoptosis.
bcl-2相关细胞凋亡的细胞内调控机制分析
基本信息
- 批准号:07670238
- 负责人:
- 金额:$ 1.28万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:1995
- 资助国家:日本
- 起止时间:1995 至 1996
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
1. Anti-apoptotic effect and the expression of p26 bcl-2 We have investigated the anti-apoptotic effect of bcl-2 proto-oncogene using bcl-2 transfectants (bcl-2 was introduced to CCRF-CEM,MBC-1, WEHI-164,2AD4) with various factor inducible apoptosis. The cells expressing a large amount of p26 bcl-2 showed higher viability when cell death was induced with H_2O_2, Dexamethasone and anti-lgM.Especially, bcl-2 has a stronger anti-apoptotic effect in the death induced with H_2O_2 than in the death induced with others. There was no significant correlation between the anti-apoptotic effect and the expression of p26 bcl-2 in the cell death induced with A23187, TNF-alpha. 2. Intarcellular events in the early phase of apoptosis and the expression of p26 bcl-2 The studies of intracellular reactive oxygen species and mitochondrial transmembrane potential of MBC-1 cells using fluorescence dye revealed no significant difference between bcl-2 transfectants and controls when cell death was induced with H_2O_2. Whereas p26 bcl-2 has significant anti-apoptotic effect in MBC-1 cells undergoing apoptosis with H_2O_2. When the transfectants of CEM-C7 cells were treated with H_2O_2, reactive oxygen species were markedly reduced but not correlate with the level of p26 bcl-2. Both intracellular reactive oxygen species and mitochondrial transmembrane potential showed no significant change in CEM,MBC-1 cells when cell death was induced with dexamethasone and anti-lgM respectively. These results suggest the anti-apoptotic effect of p26 bcl-2 has some direct relation to reactive oxygen species in early phase of apoptosis.
1. bcl-2转染CCRF-CEM、MBC-1、WEHI-164、2AD4后,通过多种因子诱导细胞凋亡,研究了bcl-2原癌基因的抗凋亡作用。H_2O_2、地塞米松和抗lgm诱导细胞死亡时,大量表达p26bcl -2的细胞存活率较高。bcl-2在H_2O_2诱导的大鼠死亡中具有较强的抗凋亡作用。在A23187、tnf - α诱导的细胞死亡中,抗凋亡作用与p26bcl -2的表达无显著相关性。2. 细胞凋亡早期细胞内事件及p26的表达bcl-2荧光染色研究发现,H_2O_2诱导细胞死亡时,bcl-2转染物与对照组细胞内活性氧和线粒体跨膜电位无显著差异。而p26 bcl-2对H_2O_2诱导的凋亡的MBC-1细胞有明显的抗凋亡作用。H_2O_2处理后,CEM-C7细胞的活性氧含量明显降低,但与p26bcl -2水平无关。地塞米松和抗lgm分别诱导CEM、MBC-1细胞死亡时,细胞内活性氧和线粒体跨膜电位均无明显变化。提示p26bcl -2的抗凋亡作用与细胞凋亡早期活性氧含量有直接关系。
项目成果
期刊论文数量(18)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Yoshihiro Komada: "Fas Receptor (CD95)-mediated apoptosis is induced in leukemic cells entering G1B compartment of the cell cycle." Blood. 86. 3848-3860 (1995)
Yoshihiro Komada:“Fas 受体 (CD95) 介导的细胞凋亡在进入细胞周期 G1B 区室的白血病细胞中被诱导。”
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Shinichi Kitada: "Reversal of chemoresistance of lymphoma cell by antisense-mediated reduction of bcl-2 gene expression" Antisense Research and Developmment. 4. 71-79 (1994)
Shinichi Kitada:“通过反义介导的 bcl-2 基因表达减少来逆转淋巴瘤细胞的化疗耐药性”反义研究与开发。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Shinichi Kitada: "Reversal of chemoresistance of lymphoma cells by antisense-mediatedreduction of bcl-2 gene expression." Antisense Research and Devlopment. 4. 71-79 (1994)
Shinichi Kitada:“通过反义介导的 bcl-2 基因表达减少来逆转淋巴瘤细胞的化疗耐药性。”
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Yoshihiro Komada et al.: "Fas Receptor (CD95) -mediated cytotoxicity is responsible for the apoptotic cell death of leukemic cells induced by interleukin-2-activated T cells." British Journal of Haematology. 96. 147-157 (1997)
Yoshihiro Komada 等人:“Fas 受体 (CD95) 介导的细胞毒性是白细胞介素 2 激活的 T 细胞诱导白血病细胞凋亡的原因。”
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- 期刊:
- 影响因子:0
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Yoshihiro Komada: "Apoptotic cell death induced by anti-lgM antibody and phorbol esters is inhibited by Interleukin-4 in human B lymphoma cell line MBC-1." Cellular Immunology. 159. 280-293 (1994)
Yoshihiro Komada:“在人 B 淋巴瘤细胞系 MBC-1 中,Interleukin-4 可抑制抗 IgM 抗体和佛波酯诱导的细胞凋亡。”
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- 影响因子:0
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