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核糖体生物发生控制部接MSC命运通过补充途径在老鼠和人类iPSC模型

Supawadee Jariyasakulroj¹, Wei Zhang², Jianhui Bai³

¹Center for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA 90033, USA; Department of Masticatory Science, Faculty of Dentistry, Mahidol University, Bangkok 10400, Thailand.

Stem cell reports

|November 17, 2023

概括

核糖体生物发生障碍会损害面发育. 通过Snord118缺陷向补体通路,揭示了一种新的机制,用于防止中细胞干细胞的骨突.

科学领域:

发展生物学发展生物学
遗传学是一个遗传学.
细胞生物学细胞生物学

背景情况:

核糖体生物生成对细胞功能至关重要,但其在面发育和突症等疾病中的作用尚未完全理解.
头骨突症涉及过早的头骨 suture 融合和 mesenchymal 干细胞 (MSCs) 的损失.

研究的目的:

为了研究Snord118的作用,Snord118是一种参与核糖体生物发生的基因,在面发育和突症中的作用.
阐明核糖体生物生成影响 suture MSC命运和部 suture发展的分子机制.

主要方法:

利用小鼠和人类诱导多能干细胞 (iPSC) 模型来研究Snord118枯竭及其对 suture MSCs的影响.
分析了p53激活,细胞死亡,增殖,分化和与核糖体蛋白和补充途径相关的基因表达.
研究了补体通路,特别是C3a受体1 (C3ar1) 在调节MSC和缺陷中的作用.

主要成果:

针MSC中的Snord118枯竭导致p53激活,增加细胞死亡,减少增殖,以及过早的骨质分化.
斯诺德118缺乏导致了核糖体蛋白的转化失调和补充通路基因的下调.
补体通路的破坏加剧了缺陷,同时激活它挽救了MSC的命运和生长,防止了骨突.

结论:

由Snord118调节的核糖体生物发生,对于维持 suture MSC命运和功能至关重要.
补体通路作为关键的调解者,将核糖体生物发生与MSC行为和面发育联系起来.
核糖体生物发生和补充通路的调节失调有助于骨突,提供潜在的治疗点.

关键词:

斯诺德118 在线观看补充路径是补充路径.头骨突突 (craniosynostosis) 是一个人类的iPSC.核糖体生物发生的生物.suture 中介细胞干细胞.

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