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富林倒置抑制了EndMT和内皮细胞的异常增殖和迁移

Rui Zeng¹, Yimin Wang², Jun Chen²

¹Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.

Clinical hemorheology and microcirculation

|May 31, 2024

概括

富林倒置抑制了氧化低密度脂蛋白诱导的内皮功能障碍,包括异常的细胞增殖,迁移和内皮到介质酶过渡 (EndMT). 这表明,氨酸是动脉样硬化病原体的关键因素.

科学领域:

心血管生物学心血管生物学
细胞生物学细胞生物学
分子医学是分子医学.

背景情况:

血管内皮在动脉样硬化心血管疾病中起着至关重要的作用.
内皮功能障碍是动脉样硬化发展的一个关键步骤.
氨酸在内皮功能障碍中的作用,特别是与内皮细胞粘附和迁移有关的作用,尚未完全理解.

研究的目的:

研究在氧化低密度脂蛋白 (ox-LDL) 诱导的内皮功能障碍中的作用.
检查氨酸对内皮细胞到介质细胞过渡 (EndMT) 和Hippo/YAP信号通路的影响.

主要方法:

用ox-LDL刺激了内皮细胞.
使用免疫光学,西部斑点和RT-qPCR评估了EndMT,furin表达和Hippo/YAP信号.
使用siRNA实现了furin敲击,以评估其对细胞增殖,迁移和EndMT的影响.

主要成果:

氧-LDL诱导的EndMT,其特征是内皮细胞和介质细胞标记物发生变化.
富林表达 (mRNA和蛋白质) 和Hippo/YAP信号被牛LDL上调.
富林倒置抑制了ox-LDL诱导的EndMT,减少了异常细胞的增殖和迁移,并恢复了内皮细胞标记物.

结论:

富林倒置减轻了ox-LDL诱导的内皮细胞异常,包括增殖,迁移和EndMT.
氨酸在内皮功能障碍中起着重要作用,可能是动脉样硬化治疗的治疗标.

关键词:

最终的MT 结束的MT 弗林·弗林·弗林,就是一个人.内皮细胞是内皮细胞.内皮质功能障碍内皮质功能障碍

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