由N6-甲基氨酸介导的circRBM33的生物发生及其在腹腔大动脉动脉瘤中的功能
Yingqi Xu1, Xiang Weng1, Jiacong Qiu1
1Department of Vascular Surgery, The Second Affiliated Hospital of Nanchang University, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Epigenetics
|September 9, 2024
概括
在腹腔大动脉动脉瘤 (AAA) 中,circRBM33 的N6-甲基氨酸 (m6A) 修饰增加. METTL3和YTHDC1通过m6A调节circRBM33的生物发生,而circRBM33的淘汰减轻了AAA的进展.
科学领域:
- 分子生物学分子生物学
- 心血管研究研究心血管研究
- 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) 是一种危及生命的疾病.
- 循环RNAs (circRNAs) 在各种疾病中发挥作用,包括AAA.
- m6A修饰在circRNA生物发生和AAA中的作用尚不清楚.
研究的目的:
- 为了研究m6A修饰对circRBM33生物生成的影响.
- 在AAA.中探索circRBM33调节的基本机制.
- 评估在AAA中准circRBM33的治疗潜力.
主要方法:
- 在体外研究中使用Ang II治疗的血管光滑肌细胞 (VSMC).
- MeRIP-PCR用于检测circRBM33.33的m6A修饰.
- 在体内AAA小鼠模型由Ang II输液诱导.
- RT-qPCR,西部斑点,HE,西里乌斯红色,以及道染色.
主要成果:
- 在Ang II诱导的VSMC中,circRBM33的m6A水平升高.
- METTL3 积极调节 circRBM33 表达; YTHDC1 缺陷降低了 circRBM33 表达.
- 通过METTL3/YTHDC1介导的m6A修饰调节circRBM33的生物发生.
- 通过减少小鼠细胞外基质 (ECM) 降解,circRBM33 knockdown减轻了AAA.
结论:
- 由METTL3/YTHDC1介导的m6A修饰调节了来自RBM33基因外型的circRBM33生物发生.
- circRBM33是通过减少ECM降解来治疗AAA的潜在治疗点.
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