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网林-4通过NF-κB信号通路促进内皮细胞中VE-cadherin的表达

Datong Zhang¹, Zhiying Zhu², Keting Wen²

¹Department of Orthodontics, School of Dentistry, Shandong University, Jinan, Shandong 250100, P.R. China.

Experimental and therapeutic medicine

|July 29, 2024

概括

内皮细胞中网氨-4 (NTN4) 的过度表达增加了血管内皮 (VE) - 原素,增强了内皮屏障. 这通过激活NF-κB信号通路发生,揭示了VE-cadherin调节的新机制.

科学领域:

内分泌学在内分泌学.
细胞生物学细胞生物学
分子生物学分子生物学

背景情况:

网林-4 (NTN4) 对于血管发育,内皮平衡和血管生成至关重要.
血管内皮质 (VE) - 阴素调节内皮细胞的迁移,增殖和透性.
在内皮细胞中NTN4和VE-cadherin之间的确切关系尚不清楚.

研究的目的:

研究NTN4过度表达对VE-cadherin在人类静脉内皮细胞 (HUVECs) 的表达的影响.
阐明涉及NTN4介导VE-cadherin调节的潜在信号通路.

主要方法:

在HUVEC中使用转感染等离子体诱导NTN4过度表达.
基因和蛋白质表达水平使用RT-qPCR和西式涂抹进行了评估.
细胞活力,迁移和透性分别使用CCK8,伤口愈合和Transwell试验进行了评估.
分析了NF-κB信号通路的激活,并使用NF-κB抑制剂证实了它的作用.

主要成果:

过度表达NTN4降低了HUVEC的活力和迁移.
VE-cadherin表达显著增加,而在NTN4过度表达时,HUVEC透性下降.
过度表达NTN4导致NF-κB蛋白水平增加,IκB-α蛋白表达减少.
抑制NF-κB消除了NTN4引起的VE-cadherin表达的增加.

结论:

过度表达NTN4通过激活NF-κB信号通路来增强HUVEC中的VE-cadherin表达.
这项研究揭示了VE-cadherin的新型调节机制.
这些发现表明NTN4是研究内皮壁相关疾病的潜在目标.

关键词:

这就是NF-κBB.它们是内皮细胞.网-4是一种透性透性的血管内皮 - - 阴素

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