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表观遗传激活的MIR100HG调节UPF1介导的氧化压力,促进肺血管免疫微环境重塑

Langlin Ou¹, Yingli Chen¹, Ao Shen¹

¹College of Medical Laboratory Science and Technology, Harbin Medical University (Daqing), Daqing, 163319, PR China.

Free radical biology & medicine

|December 6, 2025

概括

这项研究确定MIR100HG是肺高血压 (PH) 的关键参与者,显示它通过调节MIR100HG/UPF1/NRF2通路来驱动氧化应激和免疫失衡,为PH提供新的治疗点.

科学领域:

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.
肺高血压研究肺高血压研究

背景情况:

氧化应激与血管改造和肺高血压 (PH) 中的免疫失衡有关.
导致PH变化的精确表观遗传机制在很大程度上是未知的.
识别新的调节途径对于理解PH病原性至关重要.

研究的目的:

识别参与PH中染色体重塑的长非编码RNA (lncRNAs).
阐明这些lncRNAs在依赖氧化应激的PH中的调节网络.
为了研究MIR100HG在PH病原发生中的作用.

主要方法:

ChIP测序用于识别差异表达的 lncRNAs.
在体外和体内研究来评估MIR100HG功能.
转录因子结合分析 (RELA).
用RNA结合测试 (质谱,RNA-pulldown,RIP) 来确定MIR100HG的目标.
单细胞测序用于免疫微环境分析.

主要成果:

MIR100HG被确定为肺动脉光滑肌细胞 (PASMCs) 中的缺氧诱导的lncRNA,与组织蛋白修饰相关.
较高的MIR100HG会促进氧化应激,PASMC的扩散和免疫微环境的改变.
转录因子RELA上调调节了MIR100HG的表达.
MIR100HG直接与UPF1结合,调节NRF2mRNA表达并减弱抗氧化剂反应.
MIR100HG通过IBSP-ITGAV相互作用影响巨细胞激活和血管免疫微环境.

结论:

在PH中,MIR100HG/UPF1/NRF2信号轴是氧化应激和PASMC扩散的关键调节器.
这一途径有助于巨细胞的招募和免疫微环境的失衡.
MIR100HG代表了早期诊断和治疗PH的潜在治疗标.

关键词:

免疫微环境是一个微环境.在MIR100HG中.氧化应激是一种氧化应激.肺高血压是一种肺高血压.这是一个超级增强器.在 UPF1 的情况下.

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