<br>程序性细胞死亡蛋白 2 样促进血管内皮细胞炎症和氧化应激,ACS Pharmacology & Translational Science

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程序性细胞死亡蛋白 2 样促进血管内皮细胞炎症和氧化应激
ACS Pharmacology & Translational Science ( IF 4.9 ) Pub Date : 2023-09-05 , DOI: 10.1021/acsptsci.3c00129
Caifeng Li ₁ , Zhao Cui ₂ , Shiwen Deng ₁ , Tong Lei ₁ , Peng Chen _{3,

4,

5} , Hongjun Yang ₁

Affiliation

程序性细胞死亡蛋白2样（PDCD2L）是细胞核和细胞质的穿梭蛋白，与核糖体生物发生有关。然而，关于PDCD2L与炎症关系的报道较少，血管内皮细胞中PDCD2L与炎症的确切关系尚未确定。因此，我们重点探讨PDCD2L与炎症的关系及其潜在机制。我们的研究结果表明 PDCD2L 是一个促炎靶点。结果表明，通过干扰PDCD2L的表达，可以减轻LPS诱导的血管内皮细胞炎症，如IL-6和IL-1β，以及粘附因子ICAM1。同时，PDCD2L的过表达可以进一步增加LPS诱导的炎症水平、ICAM1和ROS的产生，降低CAT、GSH/GSSG水平，并增加SOD水平。因此，我们确定PDCD2L对血管内皮细胞的炎症和氧化应激具有调节作用，其调节机制可能与炎症转录因子STAT1、NF-κB调节、炎症信使mRNA的转运以及核糖体生物合成有关。然后，我们筛选出穿心莲内酯（Andro）可以与PDCD2L结合，从而抑制PDCD2L过表达引起的炎症和内皮细胞粘附。该研究揭示PDCD2L是一个潜在的抗炎治疗靶点，为抗炎药物的开发提供了新的探索。

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Programmed Cell Death Protein 2-like Promotes Inflammation and Oxidative Stress in Vascular Endothelial Cells

Programmed cell death protein 2-like (PDCD2L) is a shuttle protein of the nucleus and cytoplasm and is related to the ribosome biogenesis. However, there are few reports on the relationship between PDCD2L and inflammation, and the exact relationship between PDCD2L and inflammation has not been determined in vascular endothelial cells yet. Accordingly, we focus on exploring the relationship between PDCD2L and inflammation and its potential mechanisms. Our research findings suggested that PDCD2L is a proinflammatory target. The result showed that, by interfering with the expression of PDCD2L, LPS-induced inflammation of vascular endothelial cells can be reduced, such as IL-6 and IL-1β, as well as the adhesion factor ICAM1. Meanwhile, overexpression of PDCD2L can further increase LPS-induced inflammation levels, ICAM1, and ROS production, reduce CAT, GSH/GSSG levels, and increase SOD levels. Therefore, we determined that PDCD2L has a regulatory effect on inflammation and oxidative stress of vascular endothelial cells, and its regulatory mechanism may be related to inflammatory transcription factors STAT1, NF-κB regulation, transport of inflammatory messenger mRNA, and ribosome biogenesis. Then, we screened that andrographolide (Andro) can bind to PDCD2L, thus inhibiting inflammation and endothelial cell adhesion caused by the overexpression of PDCD2L. This study reveals that PDCD2L is a potential anti-inflammatory therapeutic target, providing new exploration for the development of anti-inflammatory drugs.

更新日期：2023-09-05

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