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暂时口激活将多能干细胞衍生的心肌细胞转化为普尔金尼纤维命运

David M Gonzalez^1,2,3,4,5, Rafael Dariolli⁶, Julia Moyett⁷

¹Department of Cell, Developmental, and Regenerative Biology, Mount Sinai, New York, NY 10029, USA.

bioRxiv : the preprint server for biology

|October 10, 2024

概括

痕信号转化人类多能干细胞衍生的心肌细胞成普金尼纤维细胞,对于理解心律失常和开发新药疗法至关重要.

科学领域:

心血管生物学心血管生物学
干细胞生物学干细胞生物学
电力生理学电力生理学

背景情况:

心脏普尔金尼纤维对于协调心脏收缩至关重要,并与心室节律失常有关.
从人类多能干细胞生成普尔金尼纤维细胞具有挑战性,限制了对导电系统缺陷的研究.

研究的目的:

为了确定参与普尔金耶纤维形成的信号通路.
研究Notch信号传导的潜力,以将人类多能干细胞衍生的心肌细胞转化为普金尼纤维细胞.

主要方法:

来自小鼠胚胎心脏的单细胞RNA测序数据的分析.
在体外激活人类多能干细胞衍生的心肌细胞中的Notch信号.
改性心肌细胞的电生理记录和RNA测序.
开发和验证用于药物反应预测的in silico模型.

主要成果:

口激活诱导了心肌细胞中的普尔金尼纤维类电生理特性和基因表达特征 (SCN5A,HCN4,ID2).
划痕诱导的细胞表现出减少的收缩力.
在 silico 模型中预测了Purkinje 纤维细胞和心肌细胞之间的差异性药物反应.
实验室验证证实了模型对抗心律失常药物疗效的预测.

结论:

痕信号传递是从人类多能干细胞产生普尔金尼纤维样细胞的关键途径.
这种新型的细胞模型有助于我们更好地理解普尔金尼纤维生理学和心脏导电障碍.
开发的in silico和in vitro模型为研究药物对心脏导电和心律失常的影响提供了一个平台.

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