在上升大动脉狭窄小鼠的左心室缩: anoikis 和进展到早期失败的进展
B Ding1, R L Price, E C Goldsmith
1Harvard-Thorndike Laboratory and the Department of Medicine, Cardiovascular Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Circulation
|June 22, 2000
概括
肌细胞亡,或编程细胞死亡,发生在心脏从缩过渡到早期失败的老鼠经历慢性生物力学压力. 这个过程可能是由anoikis触发的,这是细胞固的破坏.
科学领域:
- 心血管研究研究心血管研究
- 细胞生物学 细胞生物学
- 病理生理学 病理生理学
背景情况:
- 在小鼠上升大动脉狭窄 (AS) 是研究从心脏缩到早期衰竭的过渡的一个模型.
- 了解这种过渡的机制对于开发治疗策略至关重要.
研究的目的:
- 在上升性大动脉狭窄 (AS) 的小鼠模型中调查亡在心脏缩进展到早期失败中的作用.
- 探索将生物力学压力与肌细胞细胞死亡联系起来的潜在机制.
主要方法:
- 雄性FVB/n小鼠接受了上升大动脉狭窄症 (AS) 的手术诱导.
- 手术后4周和7周评估了心脏结构和功能.
- 使用现场结末端标记 (TUNEL) 和DNA梯级来评估肌细胞亡.
主要成果:
- 与对照组相比,AS小鼠的左心室重量与体重比率和肌细胞宽度增加.
- 到了第7周,AS肌细胞出现了分支,改变了间隔盘,以及β-1-整蛋白染色的变化.
- 通过发达的压力和分数缩短来评估心脏功能,在7周的AS小鼠中被抑制.
- 在7周的AS小鼠中检测到肌细胞亡,但在对照或4周的AS小鼠中没有检测到.
结论:
- 肌细胞亡是在慢性生物力学压力下从心脏缩过渡到早期衰竭期间出现的.
- 这些发现支持这样一个假设,即肌细胞定中的破坏,可能会在AS中启动亡.
- 这项研究阐明了一种潜在的细胞机制,有助于心力衰竭的进展.
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