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运动诱导的内皮Mecp2乳化通过Ereg/MAPK信号通路抑制动脉样硬化

Yanan Wang¹, Liangqi Chen¹, Meiju Zhang¹

¹Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China; The Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin, China.

Atherosclerosis

|May 28, 2023

概括

运动增强了乳化,这是一个翻译后的修改,有助于减少动脉样硬化. 这项研究揭示了运动诱导的乳糖化如何通过调节关键的炎症和内皮标志物来保护心血管疾病.

科学领域:

生物化学生物化学
心血管生物学心血管生物学
分子生物学分子生物学

背景情况:

乳化是一种新发现的翻译后修饰 (PTM),对生理和病理过程至关重要.
运动可以保护心血管疾病,但其对乳糖和动脉样硬化的影响尚不清楚.

研究的目的:

调查运动诱导乳糖化对动脉样硬化心血管疾病 (ASCVD) 的影响.
阐明运动通过乳化介导的抗动脉样硬化作用的潜在分子机制.

主要方法:

利用高脂肪饮食诱导的ASCVD小鼠模型.
在大动脉组织和内皮细胞中分析了蛋白质乳化,基因表达 (VCAM-1, ICAM-1, MCP-1, IL-1β, IL-6, eNOS) 和信号通路 (MAPK) 的变化.
使用RNA测序和ChIP-qPCR来识别乳基化Mecp2.2的下游标.

主要成果:

运动训练增加了Mecp2 lysine乳化 (Mecp2k271la) 和减少了动脉样性标记物,同时增加了老鼠大动脉中的eNOS.
发现Mecp2k271la通过与其染色素结合来抑制Epiregulin (Ereg) 表达,确定Ereg是关键的下游调解者.
基调节MAPK通路,影响内皮细胞功能,促进动脉样硬化回归. 外源乳酸的使用模仿了这些效应.

结论:

建立了运动和乳化之间的机械联系,突出了它在PTM中的作用.
运动诱导的乳糖化为体力活动的抗动脉样硬化益处提供了一个新的机制.
这为潜在的治疗策略提供了新的见解,针对ASCVD治疗的乳化.

关键词:

动脉样硬化是一种动脉样硬化.运动运动运动.乳母乳化乳母乳化乳母乳化这就是Mecp2的意义.后翻译修改后的修改.

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