相关实验视频
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Transverse Aortic Constriction in Mice
Published on: April 21, 2010
针对性过度表达的跨膜瘤亡因子会引起一个集中的心脏过度缩的表型
Ziad I Dibbs1, Abhinav Diwan, Shintaro Nemoto
1Winters Center for Heart Failure Research, Houston, TX 77030, USA.
Circulation
|August 13, 2003
概括
跨膜瘤亡因子 (TNF) 导致心脏肌肉变厚. 它的分泌导致心脏扩张,这表明TNF处理是心肌病的关键.
科学领域:
- 心血管生物学 心血管生物学
- 分子医学是分子医学.
- 心脏病理生理学 心脏病理生理学
背景情况:
- 瘤亡因子 (TNF) 存在于跨膜和分泌形式.
- 已知分泌的TNF对心脏的影响;跨膜TNF对心脏的作用尚不清楚.
- TNF-α转化酶 (TACE) 将跨膜TNF切割成其分泌形式.
研究的目的:
- 研究跨膜TNF对心脏的影响.
- 确定抑制TNF分泌是否可以防止心脏扩张.
主要方法:
- 产生了具有心脏特异性跨膜TNF的转基因小鼠.
- 使用TACE抑制剂治疗心脏特异性可切割TNF的小鼠.
- 评估心脏表型,肌细胞大小和基因表达.
主要成果:
- 表达非可切割的跨膜TNF的转基因小鼠发生了同心缩.
- 在具有可切割TNF的小鼠中,TACE抑制阻止了LV扩张并诱导了过度缩小.
- 超膜TNF过度表达导致心脏集中性缩.
结论:
- 跨膜TNF在心脏中具有生物活性.
- 对于发展扩张性心肌病来说,TNF处理和分泌是至关重要的.
- 针对TNF处理可能为心脏病提供治疗策略.
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