萨科等离子体网膜功能的发育编程改善了乌的心脏无氧耐受性
Ilan M Ruhr1,2, Holly A Shiels1, Dane A Crossley3
1Division of Cardiovascular Sciences, School of Medical Sciences, University of Manchester, Manchester M13 9NT, UK.
The Journal of experimental biology
|September 9, 2024
概括
抓的胚胎缺氧通过改变心脏细胞中的处理来改善成人心脏功能. 这种发育编程增强了心脏无氧耐受性,提供了一个独特的抗压现象型.
科学领域:
- 心血管生理学心血管生理学
- 发展生物学 发展生物学
- 比较生理学比较生理学
背景情况:
- 胚胎缺氧会导致持久的心脏缺陷.
- 然而,发育性缺氧可能会在一些ectotherms中产生耐压表型.
- 在发育过程中暴露于缺氧的鱼在化后表现出增强的心脏缺氧耐受性.
研究的目的:
- 为了调查通过肉质细胞网 (SR) 循环的改变 (Ca2+) 是否构成突破的发育编程心脏表型的基础.
- 确定SR函数在低氧条件下发育的海中观察到的增强无氧耐受性中的作用.
主要方法:
- 来自幼 (Chelydra serpentina) 的分离心肌细胞在正常氧化 (21% O2) 或慢性缺氧 (10% O2) 中发展.
- 细胞经受SR Ca2+循环抑制剂或没有SR Ca2+循环抑制剂的无氧/低氧化.
- 同时测量细胞缩短,细胞内Ca2+度 ([Ca2+]i) 和细胞内pH值 (pHi).
主要成果:
- 低毒性发育 (H10) 心肌细胞在诺莫克西亚下表现出较小的Ca2+过渡体和较弱的SR抑制效应,与诺莫克西亚发育 (N21) 细胞相比.
- 在这两组中,无氧抑制了心脏功能,但H10细胞显示缩短和[Ca2+]i的恢复,部分原因是肌纤维Ca2+敏感度增加.
- SR阻塞取消了H10细胞的恢复,表明SR功能在赋予无氧耐受性方面发挥了关键作用.
结论:
- 发育性缺氧永久地编程了细胞晶网膜 (SR) 功能,以打破的心脏.
- 这种编程通过修改SR功能和增加肌纤维Ca2+灵敏度来增强心脏无氧耐受性.
- 该研究提供了SR编程对优越,持久的无氧耐受性心脏表型的第一个证据.
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