bcl-2基因产物可以防止心室肌细胞的编程细胞死亡
L A Kirshenbaum1, D de Moissac
1Institute of Cardiovascular Sciences, St Boniface General Hospital Research Centre, Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada. Lorrie@SBRC.umanitoba.ca
Circulation
|October 7, 1997
概括
抗瘤蛋白bcl-2可以防止心肌细胞中由p53.3触发的细胞死亡. 这项研究证明了bcl-2的存在.
科学领域:
- 心血管生物学 心血管生物学
- 分子生物学分子生物学
- 细胞死亡研究 细胞死亡研究
背景情况:
- 编程细胞死亡 (细胞亡) 在心肌中至关重要.
- 已知p53是各种细胞类型中亡的诱导剂.
- 在预防心脏肌细胞亡中BCL-2的作用需要研究.
研究的目的:
- 确定抗亡蛋白bcl-2是否可以防止心肌细胞 (心室肌细胞) 中的p53诱导的亡.
主要方法:
- 利用复制缺陷的腺病毒将bcl-2和p53基因输送到心室肌细胞中.
- 使用生命染色评估肌细胞细胞死亡.
- 通过DNA碎片化和终端转移酶脱氧核酸末端标记评估的亡.
- 测量了巴克斯促进体转录水平.
主要成果:
- p53显著增加了心室肌细胞死亡和亡.
- p53还增加了巴克斯促进体转录.
- bcl-2表达阻止了p53诱导的肌细胞死亡和亡.
- bcl-2抑制了p53依赖的巴克斯转录.
结论:
- bcl-2 在心室肌细胞中起到抗亡因子的作用.
- 这是BCL-2在心肌细胞中的抗亡作用的首个证据.
- bcl-2的保护作用与抑制p53介导的巴克斯转录有关.
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