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Zbtb16通过IGF2BP3介导的mRNA稳定来确定心血管原始体的命运可塑性

Wuchan Wang¹, Yilin Lian¹, Jianguo Li¹

¹Clinical and Translational Research Center of Shanghai First Maternity and Infant Hospital, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Key Laboratory of Signaling and Disease Research, Frontier Science Center for Stem Cell Research, National Stem Cell Translational Resource Center, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China.

|August 8, 2025

概括

Zbtb16蛋白调节心血管原生细胞的命运. 它的缺失会重定向细胞发育,影响心脏功能,并可能导致心室非紧缩.

科学领域:

心血管生物学心血管生物学
干细胞研究的研究.
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

心血管前体 (CPs) 产生多种心脏细胞,但它们的命运可塑性机制尚不清楚.
在CP亚群中存在转录异质性.

研究的目的:

调查ZBTB家族蛋白质Zbtb16在调节心血管前体 (CP) 亚种群命运可塑性的作用.
阐明了Zbtb16介导的CP差异化调节背后的分子机制.

主要方法:

来自多能干细胞的三个CP亚群的特征.
分析Zbtb16删除对CP分化轨迹的影响.
研究Zbtb16与IGF2BP3的相互作用及其在mRNA稳定中的作用.

主要成果:

Zbtb16删除将早期CP从心肌细胞 (CM-CP) 重定向到内皮细胞/心脏纤维细胞 (EC/CF-CP) 谱系.
这种重定向可能会导致小鼠心室不紧缩和心脏功能受损.
Zbtb16与m6A阅读器IGF2BP3相互作用,以稳定CM-CP确定至关重要的mRNA.

结论:

Zbtb16是异质CP亚群中命运可塑性的关键调节者.
Zbtb16和IGF2BP3的相互作用影响m6A修饰的mRNA稳定.
结果提供了关于心血管多系系命运决定和CP可塑性的见解.

关键词:

科普:分子生物学分子生物学科普:干细胞研究在 IGF2BP3BP3 中.在 Zbtb1616 的位置上.心血管疾病的前身.命运塑性运气塑性稳定 mRNA 的稳定.

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