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与SCD1相关的表观遗传修饰会影响心肌细胞中激素敏感脂酶 (Lipe) 基因表达

Adam Olichwier¹, Adrian Sowka¹, Volodymyr V Balatskyi¹

¹Laboratory of Molecular Medical Biochemistry, Nencki Institute of Experimental Biology of Polish Academy of Sciences, Warsaw, Poland.

Biochimica et biophysica acta. Molecular cell research

|October 18, 2023

概括

基CoA脱酶1 (SCD1) 调节心脏脂解和表观遗传修饰. 抑制SCD1影响DNA甲基化和激素敏感脂酶 (Lipe) 表达,影响心肌细胞对缺氧的反应.

科学领域:

心血管生物学心血管生物学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
代谢调节代谢调节代谢调节

背景情况:

基CoA脱酶1 (SCD1) 对于心脏中的脂解和表观遗传调节至关重要.
表观遗传修饰和脂质代谢转变是心脏对缺氧反应的关键.
在不同氧气条件下的心肌细胞中SCD1,表观遗传学和脂解之间的相互作用需要研究.

研究的目的:

研究SCD1和表观遗传修饰在控制心肌细胞脂解中的相互作用.
确定SCD1在规范DNA甲基化和基因表达中的作用,在正常和缺氧条件下.

主要方法:

使用HL-1心肌细胞和小鼠心脏模型.
评估了SCD1活性,DNA甲基化水平,DNA甲基转移酶 (DNMT) 活性以及DNMT1和激素敏感脂酶 (Lipe) 的表达.
研究了SCD1抑制和缺氧对表观遗传标记和基因表达的影响,包括缺氧诱导因子1α.

主要成果:

抑制SCD1降低了全球DNA甲基化,DNMT活性和DNMT1在心肌细胞和小鼠心脏中的表达.
抑制SCD1导致Lipe基因促进物的甲基化增加,减少Lipe的表达.
在低氧状态下,SCD1抑制减弱了DNMT1的DNA低甲基化,并通过Lipe促进物去甲基化促进了Lipe表达.

结论:

SCD1在控制心脏内表观遗传机制方面发挥着重要作用.
SCD1通过调节其促进体甲基化来影响Lipe表达.
SCD1是心肌细胞对正常氧和缺氧的表观遗传反应的关键因素.

关键词:

乙化乙化是一种在DNMT中使用DNMT.表观遗传修饰表观遗传修饰表观遗传修饰这就是HIF1α.氧气过低是因为缺氧.甲基化甲基化甲基化诺尔莫克西亚 (Normoxia) 是一个常见的药物.

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