Regulation of Histone Acetylation on Expression Profiles of Potassium Channels During Cardiomyocyte Differentiation From Mouse Embryonic Stem Cells
Regulation of Histone Acetylation on Expression Profiles of Potassium Channels During Cardiomyocyte Differentiation From Mouse Embryonic Stem Cells
复制标题
组蛋白乙酰化对小鼠胚胎干细胞心肌细胞分化过程中钾通道表达谱的调节
DOI：
10.1002/jcb.26102
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发表时间：
2017
影响因子：
4
通讯作者：
Peng Luying
中科院分区：
文献类型：
--
作者：
Wang Duo;Liu Chang;Li Zhigang;Wang Yumei;Wang Wenjing;Wu Xiujuan;Wang Kang;Miao Wei;Li Li;Peng Luying
The cardiomyocyte differentiation from mouse embryonic stem cells (mESCs) is a dynamic and complex process that involved in the precision regulation of histone acetylation. The formation of action potential (AP) in mature cardiomyocytes is based on the expression pattern of Na+, Ca2+, and K+ ion channels, in which the slow delayed rectifier potassium current (IKs), the rapid delayed rectifier potassium current (IKr) and the inwardly rectifying Kir current (IK1) mainly contribute to repolarization for AP in different species. However, the expression status of potassium channels conducted IKs, IKr, and IK1 in cardiomyocyte differentiation are not fully defined. Here, we investigated the expression pattern of the slow delayed rectifier potassium channel and the rapid delayed rectifier potassium channel using a model of mouse cardiomyocyte differentiation under different conditions of histone acetylation. We found that expression levels of both the delayed rectifier potassium channel and the inwardly rectifying potassium channel were more sensitive to histone hyperacetylation during differentiation from mESCs into cardiomyocytes. Especially, histone H4 hyperacetylation induced by Class I HDACs inhibitors promoted the expression profiles of potassium channels (Kcnj2, Kcnj3, Kcnj5, Kcnj11, and Kcnh2) in the process. Our results provide a clue for expression status of potassium channels which may be essential to forming functional cardiomyocyte in the cardiac lineage commitment of mESC. J. Cell. Biochem. 118: 4460–4467, 2017. © 2017 Wiley Periodicals, Inc.
