The effect of miR-223-3p on endothelial cells in coronary artery disease

作者：Zhao, Boxin; Zang, Yunhui; Gui, Lin; Xiang, Yingyu; Zhang, Zhiyong; Sun, Xueyuan; Fan, Jingyao; Huang, Lijuan^*

来源：In Vitro Cellular and Developmental Biology - Animal, 2023.

DOI：10.1007/s11626-023-00842-7

• Endothelial cells
• microRNA-223-3p
• KLF15
• Apoptosis

Endothelial cell damage and dysfunction are crucial factors in the development and early stages of coronary artery disease (CAD) and apoptosis plays a significant role in this process. In this study, We aimed to simulate the CAD vascular microenvironment by treating endothelial cells with tumor necrosis factor alpha (TNF-alpha) to construct an endothelial cell apoptosis model. Our findings revealed that the TNF-alpha model resulted in increased micro-RNA 223-3p (miR-223-3p) mRNA and Bax protein expression, decreased kruppel-like factor 15 (KLF15) and Bcl-2 protein expression, and decreased cell viability. More importantly, in the TNF-alpha-induced endothelial cell apoptosis model, transfection with the miR-223-3p inhibitor reversed the effects of TNF-alpha on Bcl-2, Bax expression. We transfected miRNA-223-3p mimics or inhibitors into endothelial cells and assessed miR-223-3p levels using RT-PCR. Cell viability was detected using CCK8. Western blot technology was used to detect the expression of Bcl-2, Bax, and KLF15. In summary, this study demonstrates the role and possible mechanism of miR-223-3p in endothelial cells during CAD, suggesting that miR-223-3p may serve as a promising therapeutic target in CAD by regulating KLF15.

• 单位
  哈尔滨医科大学