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首页> 外文期刊>Cell cycle >IRX1 hypermethylation promotes heart failure by inhibiting CXCL14 expression
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IRX1 hypermethylation promotes heart failure by inhibiting CXCL14 expression

机译：IRX1高甲基化通过抑制CXCL14表达来促进心力衰竭

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摘要

To identify the mechanism and functions of IRX1 in heart failure (HF) and provide evidence for new therapies. Bioinformatic analysis was performed to select target genes in HF cells compared to normal groups. Experimental rats were treated in a controllable manner to explore how IRX1 methylation accounted for this disease in vivo. Cardiac ultrasonic and morphologic examinations were conducted to test the mouse heart and evaluate the degree of cardiac impairment at in the level of organization. GSEA analysis revealed the relative enrichment of functions. Immunofluorescent assays, western blotting and qRT-PCR were used to determine the DNA methylation and expression levels. IRX1 was hypermethylated in heart failure and identified as a target gene by bioinformatic analysis. Transverse aortic constriction (TAC) induced heart failure in rats, while 5-aza-2MODIFIER LETTER PRIME-deoxycytidine (5-Aza) alleviated heart failure in rats according to medical cardiac indexes. Western blotting and qRT-PCR revealed that a conspicuous difference in the expression of IRX1 and CXCL14 between HF and normal cardiac cells. As a result of gene methylation, left ventricular hypertrophy and cardiac fibrosis is usually accompanied by heart failure. Moreover, is the results implied that the demethylation of IRX1 improves heart failure in vivo and in vitro. IRX1 methylation induced damaged cardiac function and even heart failure, which has important implications for HF treatment and diagnosis.
机译：确定IRX1在心力衰竭（HF）中的机制和功能，并为新疗法提供证据。与正常组相比，进行生物信息分析以在HF细胞中选择靶基因。实验大鼠以可控的方式处理，以探讨IRX1甲基化如何在体内占该疾病。进行了心脏超声波和形态学检查以测试小鼠心脏并评估组织水平的心脏损伤程度。 GSEA分析揭示了功能的相对富集。免疫荧光测定，用于确定DNA甲基化和表达水平的蛋白质印迹和QRT-PCR。 IRX1在心力衰竭中高甲基化，并通过生物信息分析鉴定为靶基因。横向性收缩（TAC）诱导大鼠心力衰竭，而5- AZA-2涂剂字母主要 - 脱氧胞苷（5-AZA）根据医疗心脏指数，大鼠的心力衰竭。蛋白质印迹和QRT-PCR显示，HF和正常心脏细胞之间IRX1和CXCL14表达的显着差异。由于基因甲基化，左心室肥大和心肌纤维化通常伴有心力衰竭。此外，结果暗示IRX1的去甲基化改善体内和体外心力衰竭。 IRX1甲基化诱导受损的心脏功能甚至心力衰竭，这对HF治疗和诊断具有重要意义。

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  • 来源
    《Cell cycle》 |2019年第23期|共12页
  • 作者

    Zeng Longhuan; Gu Nanyuan; Chen Jiayi; Jin Guangyong; Zheng Yongke;

  • 作者单位

    Zhejiang Univ Sch Med Affiliated Hangzhou Peoples Hosp 1 Dept Intens Care Unit 261 Huansha Rd;

    Zhejiang Univ Sch Med Affiliated Hangzhou Peoples Hosp 1 Dept Intens Care Unit 261 Huansha Rd;

    Zhejiang Univ Sch Med Affiliated Hangzhou Peoples Hosp 1 Dept Intens Care Unit 261 Huansha Rd;

    Zhejiang Univ Sch Med Affiliated Hangzhou Peoples Hosp 1 Dept Intens Care Unit 261 Huansha Rd;

    Zhejiang Univ Sch Med Affiliated Hangzhou Peoples Hosp 1 Dept Intens Care Unit 261 Huansha Rd;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    DNA methylation; heart failure; 5-aza-2'-deoxycytidine;

    机译：DNA甲基化;心力衰竭;5-AZA-2'-脱氧胞苷;

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