INSERM U-1251, MMG, Aix-Marseille University, Marseille, 13885, France.
Istituto di Ricerca Genetica e Biomedica, UOS di Milano, CNR, Rozzano, 20138, Italy.
Nat Commun. 2019 Apr 26;10(1):1929. doi: 10.1038/s41467-019-09459-5.
Genetically modified mice have advanced our understanding of valve development and disease. Yet, human pathophysiological valvulogenesis remains poorly understood. Here we report that, by combining single cell sequencing and in vivo approaches, a population of human pre-valvular endocardial cells (HPVCs) can be derived from pluripotent stem cells. HPVCs express gene patterns conforming to the E9.0 mouse atrio-ventricular canal (AVC) endocardium signature. HPVCs treated with BMP2, cultured on mouse AVC cushions, or transplanted into the AVC of embryonic mouse hearts, undergo endothelial-to-mesenchymal transition and express markers of valve interstitial cells of different valvular layers, demonstrating cell specificity. Extending this model to patient-specific induced pluripotent stem cells recapitulates features of mitral valve prolapse and identified dysregulation of the SHH pathway. Concurrently increased ECM secretion can be rescued by SHH inhibition, thus providing a putative therapeutic target. In summary, we report a human cell model of valvulogenesis that faithfully recapitulates valve disease in a dish.
基因修饰小鼠促进了我们对瓣膜发育和疾病的理解。然而,人类的病理生理学瓣膜发生仍知之甚少。在这里,我们报告了通过单细胞测序和体内方法,可以从多能干细胞中获得一群人胚前期心内膜细胞(HPVCs)。HPVCs 表达的基因模式符合 E9.0 小鼠房室管(AVC)心内膜的特征。用 BMP2 处理的 HPVCs,在鼠 AVC 垫上培养,或移植到胚胎鼠心脏的 AVC 中,经历内皮到间充质的转变,并表达不同瓣膜层的瓣膜间质细胞标志物,显示出细胞特异性。将该模型扩展到患者特异性诱导多能干细胞中,重现了二尖瓣脱垂的特征,并确定了 SHH 途径的失调。同时,通过 SHH 抑制可以挽救 ECM 分泌的增加,从而提供了一个潜在的治疗靶点。总之,我们报告了一种瓣膜发生的人类细胞模型,在体外忠实地再现了瓣膜疾病。