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Transverse Aortic Constriction in Mice
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在缺乏内皮氧化合成酶的小鼠中,心力衰竭和先天性隔膜缺陷的发展
Qingping Feng1, Wei Song, Xiangru Lu
1Department of Medicine, London Health Sciences Centre, London, Ontario, Canada. qfeng@uwo.ca
Circulation
|August 15, 2002
概括
内皮氧化合成酶 (eNOS) 缺乏导致老鼠的死亡率增加和先天性心脏缺陷,包括隔膜缺陷. 这与心脏发育期间心肌细胞亡的升高有关.
科学领域:
- 心血管生物学 心血管生物学
- 发展生物学 发展生物学
- 分子心脏病学分子心脏病学
背景情况:
- 内皮氧化合成酶 (eNOS) 对于调节细胞生长,细胞亡和组织输液至关重要.
- 以前的研究表明,缺乏eNOS的小鼠表现出异常的大动脉双门.
- eNOS在心脏发育中的作用需要进一步研究.
研究的目的:
- 研究eNOS在心脏发育中的作用.
- 评估eNOS缺乏对心脏功能和存活率的影响.
主要方法:
- 检查了生后死亡率,心脏功能和面膜缺陷的eNOS(-/-),eNOS(+/-) 和野生型小鼠.
- 使用超声波晶体来测量心脏缩短.
- 在胚胎和新生儿阶段评估心肌细胞亡和caspase-3活性.
主要成果:
- 与野生类型 (13.3%) 相比,eNOS(-/-) (85.1%) 和eNOS(+/-) (38.3%) 小鼠的产后死亡率显著增加.
- 在ENOS缺乏的小鼠中发现严重的肺堵塞和心脏缩短的减少.
- 在eNOS(-/-) (75%) 和eNOS(+/-) (32.4%) 的新生儿中,心房和心室隔膜缺陷显著增加,而野生型 (4.9%) 则显著增加.
- 在eNOS的胚胎和新生儿中观察到心肌细胞亡和caspase-3活性增加.
结论:
- 在心脏发育过程中,eNOS缺乏导致心力衰竭和先天性隔膜缺陷.
- 增加心肌细胞亡与eNOS缺乏和心脏异常有关.
- eNOS对于正常的心脏发育至关重要.
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