内甲素-1 影响hiPSC衍生的心肌细胞的机械性质和收缩性,从而导致扩张性功能障碍

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Caterina Redwanz¹, Ricardo H Pires², Doreen Biedenweg²

¹Department for Internal Medicine B, Cardiology, University Medicine Greifswald, Ferdinand-Sauerbruch-Straße, 17475 Greifswald, Germany; German Centre for Cardiovascular Research (DZHK), partner site Greifswald, Ferdinand-Sauerbruch-Straße, 17475 Greifswald, Germany.

Journal of molecular and cellular cardiology

|July 17, 2024

概括

人类诱导的多能干细胞衍生心肌细胞 (hiPSC-CMs) 的内末林-1 (ET-1) 治疗导致硬度增加和放松功能受损,为扩张功能障碍研究提供了一个新模型.

科学领域:

心血管生物学心血管生物学
干细胞研究干细胞研究
细胞力学细胞力学

背景情况:

扩张性功能障碍显著影响患者的生活质量.
了解其病理机制是开发有效疗法的关键.
人类诱导的多能干细胞衍生心肌细胞 (hiPSC-CMs) 提供了一个有前途的模型系统.

研究的目的:

为了研究内甲素-1 (ET-1) 对hiPSC-CMs的影响.
检查ET-1诱导的心肌细胞机制和收缩能力的变化,特别是放松.
探索ET-1影响背后的分子机制.

主要方法:

在24小时和48小时内,hiPSC-CM患者接受了10nM ET-1的治疗.
实时变形性细胞计 (RT-DC) 评估了细胞大小和机械性质.
阶段对比视频显微镜评估了收缩行为.
在NanoString nCounter®心血管疾病小组分析了基因表达.

主要成果:

治疗ET-1导致心肌细胞大小增加 (过度缩小).
接受ET-1治疗的hiPSC-CMs表现出增加的刚性和受损的放松.
基因表达分析揭示了与心血管疾病,超和细胞外基质相关的途径的上调,与脂肪酸代谢途径的下调.

结论:

在hiPSC-CMs中ET-1诱导的变化超出了简单的缩.
这些变化包括细胞力学和收缩功能的显著修改.
接受ET-1治疗的hiPSC-CMs代表了一种有价值的体外模型,用于研究透缩功能障碍.

关键词:

细胞力学细胞力学扩张性功能障碍扩张性功能障碍输内甲林-1-1是什么 hiPSC的心肌细胞

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