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缺乏MCPIP1可以通过抑制MAPK信号传递来缓解腹腔大动脉动脉瘤的形成

Ming Xue¹, Hailing Ding², Yongxin Han³

¹Department of Interventional Radiology, Weihai Municipal Hospital, Cheeloo College of Medicine, Shandong University, Weihai, Shandong 264200, P.R. China.

Biochemistry and cell biology = Biochimie et biologie cellulaire

|June 6, 2025

概括

单细胞化疗蛋白诱导蛋白-1 (MCPIP1) 缺陷通过防止血管光滑肌细胞变化和MAPK通路激活,减少腹腔大动脉动脉瘤 (AAA) 的形成. KLF4调节MCPIP1,影响AAA的发展.

科学领域:

血管生物学血管生物学
分子医学是分子医学.
心血管研究研究心血管研究

背景情况:

腹腔大动脉动脉瘤 (AAA) 是一种严重的大动脉疾病.
单细胞化疗蛋白诱导蛋白-1 (MCPIP1) 与AAA病变发生有关.
MCPIP1在 angiotensin II (Ang II) 诱导的AAA中的确切作用尚不清楚.

研究的目的:

研究MCPIP1在Ang II诱导的AAA形成中的特定作用.
阐明MCPIP1影响血管光滑肌细胞 (VSMC) 和相关信号通路的分子机制.

主要方法:

利用Ang II诱导的AAA的小鼠模型.
在MCPIP1缺乏和野生型小鼠中评估了AAA形成,原/弹性质降解和VSMC标记 (αSMA,SM22α).
分析了基激活蛋白激酶 (MAPK) 信号通路和VSMC增殖/迁移.
通过使用光酶和ChIP试验,研究了KLF4对MCPIP1的转录调节.

主要成果:

在接受Ang II治疗的小鼠中,MCPIP1缺乏显著降低了AAA形成和细胞外基质降解.
缺乏MCPIP1保留了αSMA和SM22α水平,并减弱了大动脉和VSMC中的MAPK信号激活.
沉默MCPIP1抑制了Ang II诱导的VSMC增殖和迁移;PD98059 (ERK1/2抑制剂) 模仿了这种效应.
证实KLF4是MCPIP1的转录调节剂,KLF4的倒置逆转了Ang II对MCPIP1表达的影响.

结论:

MCPIP1促进了Ang II诱导的AAA形成.
通过MAPK信号通路,MCPIP1促进了VSMC表型切换和细胞外矩阵降解.
在Ang II诱导的AAA的背景下,KLF4在调节MCPIP1表达方面发挥着至关重要的作用.

关键词:

在MAPK信号传输中.在MCPIP1中,MCPIP1是MCPIP1.腹部大动脉动脉瘤腹部大动脉动脉瘤现象型切换的切换血管光滑肌肉细胞的细胞.

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