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甲基-CpG结合 2 K271乳介导的M2巨细胞两极化抑制动脉样硬化

Liangqi Chen^1,2, Meiju Zhang^1,2, Xueyan Yang^1,2

¹Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.

|August 8, 2024

概括

运动通过促进MeCP2乳化来改善动脉样硬化,从而增强M2巨细胞两极化和斑块稳定性. 这项研究确定了RUNX1作为心血管疾病的基于运动的干预措施的潜在治疗标.

科学领域:

分子生物学和生物化学分子生物学和生物化学
心血管研究研究心血管研究
表观遗传学和翻译后修改

背景情况:

蛋白质翻译后修改在运动诱导的对动脉样硬化的心脏保护中的作用仍然在很大程度上未被探索.
动脉样性心血管疾病 (ASCVD) 是一个主要的全球健康问题,需要新的治疗策略.
了解运动有益作用的分子机制,可以揭示ASCVD治疗的新目标.

研究的目的:

通过蛋白质乳糖化研究运动介导的动脉样硬化改善的新机制.
为了确定特定的运动诱导的乳化部位及其对斑块稳定性的功能影响.
探索向乳化通路和相关因子 (如RUNX1) 的潜力,用于治疗干预.

主要方法:

在ApoE-/-小鼠中进行蛋白质组学分析,这些小鼠接受了运动方案,以确定运动诱导的乳化.
在斑块巨细胞中MeCP2 K271乳化部位和腺病毒转移的部位导向突变发生.
ATAC-Seq,CUT &Tag,以及分子生物学技术,以阐明分子机制;药理上抑制RUNX1.

主要成果:

运动诱导的甲基-CpG结合蛋白2 (MeCP2) 在大动脉斑块巨细胞中的lysine 271 (K271) 的特定乳化.
MeCP2 K271乳化促进了M2巨细胞的偏离,减少了斑块面积,死核和脂质沉积,同时增加了原蛋白含量.
通过MeCP2 K271乳化和H3K36me3相互作用确定了RUNX1转录抑制作为关键机制;RUNX1抑制显示了atheroprotective效应.

结论:

运动通过一种新的MeCP2 K271乳化-H3K36me3/RUNX1通路改善动脉样硬化.
增强MeCP2 K271乳化促进M2巨细胞的透,稳定斑块,并降低ASCVD风险.
在ASCVD中,RUNX1被验证为运动模拟疗法的潜在治疗标.

关键词:

H3K36me3是什么意思 H3K36me3是什么意思在MeCP2中,乳酸化是MeCP2的重要组成部分.动脉样硬化动脉样硬化染色质可访问性染色质可访问性运动就是炼身体.巨细胞的两极分化

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