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胰岛细胞转录因子 1 与 GCN5 协同作用促进间充质干细胞向心肌细胞分化。

Islet-1 synergizes with Gcn5 to promote MSC differentiation into cardiomyocytes.

机构信息

Department of Clinical Laboratory; Ministry of Education Key Laboratory of Child Development and Disorders; National Clinical Research Center for Child Health and Disorders (Chongqing); China International Science and Technology Cooperation base of Child development and Critical Disorders; Children's Hospital of Chongqing Medical University, Chongqing, P.R. China.

Department of Pediatric Research Institute, Ministry of Education Key Laboratory of Child Development and Disorders; National Clinical Research Center for Child Health and Disorders (Chongqing); China International Science and Technology Cooperation base of Child development and Critical Disorders; Children's Hospital of Chongqing Medical University, Chongqing, P.R. China.

出版信息

Sci Rep. 2020 Feb 4;10(1):1817. doi: 10.1038/s41598-020-58387-8.

Abstract

Mesenchymal stem cells (MSCs) specifically differentiate into cardiomyocytes as a potential way to reverse myocardial injury diseases, and uncovering this differentiation mechanism is immensely important. We have previously shown that histone acetylation/methylation and DNA methylation are involved in MSC differentiation into cardiomyocytes induced by islet-1. These modifications regulate cardiac-specific genes by interacting with each other in the promoter regions of these genes, but the molecular mechanism of these interactions remains unknown. In this study, we found that the key enzymes that regulate GATA4/Nkx2.5 expression are Gcn5/HDAC1, G9A, and DNMT-1. When α-methylene-γ-butyrolactone 3 (MB-3) was used to inhibit Gcn5 expression, we observed that the interactions among these key enzymes in the GATA4/Nkx2.5 promoters were blocked, and MSCs could not be induced into cardiomyocytes. Our results indicated that islet-1 could induce Gcn5 binding to GATA4/Nkx2.5 promoter regions and induce the interactions among Gcn5, HDAC1, G9A and DNMT-1, which upregulated GATA4/Nkx2.5 expression and promoted MSC differentiation into cardiomyocytes.

摘要

间充质干细胞(MSCs)可特异地分化为心肌细胞,这是逆转心肌损伤疾病的一种潜在方法,因此揭示这种分化机制非常重要。我们之前已经表明,组蛋白乙酰化/甲基化和 DNA 甲基化参与了胰岛-1诱导的 MSC 向心肌细胞的分化。这些修饰通过在这些基因的启动子区域相互作用来调节心脏特异性基因,但这些相互作用的分子机制尚不清楚。在这项研究中,我们发现,调节 GATA4/Nkx2.5 表达的关键酶是 Gcn5/HDAC1、G9A 和 DNMT-1。当使用α-亚甲基-γ-丁内酯 3(MB-3)抑制 Gcn5 的表达时,我们观察到这些关键酶在 GATA4/Nkx2.5 启动子中的相互作用被阻断,MSCs 不能被诱导为心肌细胞。我们的结果表明,胰岛-1 可以诱导 Gcn5 结合到 GATA4/Nkx2.5 启动子区域,并诱导 Gcn5、HDAC1、G9A 和 DNMT-1 之间的相互作用,从而上调 GATA4/Nkx2.5 的表达,并促进 MSC 向心肌细胞分化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a090/7000709/fa5cd40d1a78/41598_2020_58387_Fig1_HTML.jpg

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