在BASP1mRNA上通过WTAP介导的m6A修改有助于AAA中的铁亡
Zexiang Tian1, Wei Li1, Jian Wang1
1Department of Cardiothoracic Surgery, The Affiliated Hospital of Inner Mongolia Medical University, No.1, Tongdao North Street, Huimin District, Hohhot, 010050, China.
General thoracic and cardiovascular surgery
|February 19, 2025
概括
大脑丰富的膜附着信号蛋白1 (BASP1) 在腹腔大动脉动脉瘤 (AAA) 中起着关键作用. WTAP蛋白调节BASP1的m6A修饰,影响AAA进展和铁亡.
科学领域:
- 心血管生物学 心血管生物学
- 分子生物学分子生物学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
背景情况:
- 腹腔大动脉瘤 (AAA) 是一种与动脉样硬化相关的危及生命的疾病.
- 大脑丰富的膜附着信号蛋白1 (BASP1) 在AAA病变发生过程中的作用目前尚不清楚.
研究的目的:
- 调查BASP1在 ангиотензин-II诱导的AAA中的作用和机制.
- 在AAA中探索BASP1和WTAP之间的监管关系.
主要方法:
- 对BASP1和WTAP的基因表达分析 (qRT-PCR,西布洛特).
- 在体外AAA模型使用血管光滑肌细胞 (VSMC) 中的 ангиотензин-II.
- 功能性测试包括细胞活力 (MTT),细胞亡 (流细胞计),氧化应激和Fe2+水平.
- 机制研究涉及MeRIP-qPCR和双 luciferase 记者试验,以评估m6A 修饰和mRNA 稳定性.
主要成果:
- 在AAA组织中,BASP1表达显著上调,在VSMC中由Ang-II诱导.
- 在BASP1 knockdown中加剧了Ang-II诱导的AAA和ferroptosis.
- 通过WTAP调解了BASP1.1的N6-甲基氨酸 (m6A) 修饰和mRNA稳定性.
- 在AAA组织中,WTAP的表达很高,其沉默效应通过BASP1上调来抵消.
结论:
- WTAP促进了VSMC的活力,并抑制了Ang-II诱导的亡和铁亡.
- WTAP通过调节BASP1的m6A水平来发挥其作用,突出了AAA的新型监管途径.
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