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通过向TAF15,NDRG1促进内皮功能障碍和缺氧诱导的肺高血压

Chengwei Li¹, Junzhu Lv¹, Gulinuer Wumaier¹

¹Department of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.

Precision clinical medicine

|October 27, 2023

概括

缺氧增加N-myc下游调节基因-1 (NDRG1) 在肺动脉内皮细胞,驱动血管改造和肺高血压. 抑制NDRG1可以通过向TAF15.5来减轻这些影响.

科学领域:

心血管研究研究心血管研究
肺部医学肺部医学
分子生物学分子生物学

背景情况:

肺高血压 (PH) 是一种严重的疾病,与慢性缺氧和血管重塑有关.
缺氧诱导的血管改造的确切机制尚不清楚.

研究的目的:

研究N-myc下游调节基因-1 (NDRG1) 在缺氧诱导的肺血管改造中的作用.
阐明NDRG1在缺氧的情况下影响内皮细胞功能的分子机制.

主要方法:

使用定量PCR,西式涂抹和免疫组织化学来评估NDRG1表达.
功能丧失 (shRNA) 和过度表达研究在人类肺动脉内皮细胞 (HPAEC) 上进行.
研究了NDRG1和TATA盒结合蛋白相关因子15 (TAF15) 之间的相互作用,以及对信号通路和体内模型的影响.

主要成果:

在低氧状态下的HPAEC和人类/大鼠肺病变中,NDRG1的表达显著增加.
抑制NDRG1降低了HPAEC的扩散,迁移和管道形成,而过度表达则增加了这些.
NDRG1与TAF15相互作用,促进其核定位,TAF15的敲击扭转了NDRG1的影响.
TAF15与PH相关的信号通路 (PI3K-Akt,p53,HIF-1) 有关.
在老鼠中,NDRG1敲击减弱了缺氧诱导的血管改造和右心室缩.

结论:

缺氧诱导的NDRG1上调有助于内皮功能障碍和肺高血压.
NDRG1针对TAF15,调解其对内皮细胞和血管重塑的影响.
NDRG1代表了缺氧诱导的肺高血压的潜在治疗标.

关键词:

N-myc下游调节的基因-1 与TATA盒结合蛋白相关的15因子相关的15因子内皮质功能障碍在内皮质功能障碍缺氧引起的肺高血压.血管改造血管改造血管改造

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