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在糖尿病视网膜病变的小鼠模型中,Nox4上调对PECAM-1表达的影响

Jinli Wang¹, Daniel A Lai¹, Joshua J Wang¹

¹Department of Ophthalmology and Ross Eye Institute, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, United States of America.

|May 15, 2024

概括

这项研究研究了NADPH氧化酶4 (Nox4) 在调节糖尿病视网膜病变中的血小板内皮细胞粘附分子1 (PECAM-1) 表达中的作用. 研究结果表明Nox4不会显著改变视网膜内皮细胞中的PECAM-1水平.

科学领域:

眼科医生眼科眼科
血管生物学血管生物学
分子医学是分子医学.

背景情况:

糖尿病视网膜病变 (DR) 导致视力丧失,由血管变化驱动.
NADPH氧化酶4 (Nox4) 活性与DR病原发生有关,特别是血管泄漏.
血小板内皮细胞粘附分子1 (PECAM-1) 影响内皮屏障功能.

研究的目的:

为了确定Nox4上调是否影响糖尿病患者视网膜中的PECAM-1表达.
研究Nox4对小鼠视网膜和大脑微血管内皮细胞 (BMECs) 中PECAM-1的影响.

主要方法:

使用内皮细胞特异的Nox4转基因 (TG) 和条件淘汰 (cKO) 鼠标.
在视网膜,BMEC和培养的人类视网膜内皮细胞 (HREC) 中检查了PECAM-1mRNA和蛋白质表达.
在HREC中使用了腺病毒介导的Nox4过度表达.

主要成果:

Nox4过度表达增加了PECAM-1mRNA,但不是视网膜,BMEC和HREC中的蛋白质.
不管糖尿病,来自Nox4 cKO小鼠的BMEC中,PECAM-1 mRNA和蛋白质水平保持不变.
这些结果不支持Nox4在调节糖尿病患者视网膜PECAM-1表达中的作用.

结论:

诺克斯4似乎没有显著调节内皮细胞或糖尿病视网膜中的PECAM-1表达.
在DR中Nox4诱导的血管泄漏背后的机制需要进一步研究,重点关注其他内皮结节蛋白.

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