• Xiaoying He, Xin Zhao, and Hongqin Wang.
• Shanxi Provincial Key Laboratory of Kidney Disease, Shanxi Provincial People's Hospital, Taiyuan, China.
• Ann. Med. 2024 Dec 1; 56 (1): 24075252407525.

IntroductionAtherosclerosis (AS) is a chronic inflammatory disease characterized by lipid accumulation, inflammation and apoptosis of the arterial wall. This study evaluated the effects of lysophosphatidylinositol (LPI) on endothelial cells activation and autophagy in AS.MethodsqRT-PCR and Western blotting were done to verify the expression of ICAM1, GPR55 and SOD2. RNA-Seq was performed and screened for the different expressions of long noncoding RNAs (lncRNAs), combining bioinformatics analysis to elucidate the mechanism by which lncRNA functions.ResultsqRT-PCR and Western blotting results showed that LPI increased GPR55 and ICAM1 expression. RNA-Seq analysis and qRT-PCR results showed that LPI increased the expression of LINC01235, LINC00520 and LINC01963; LINC01235 was the most obvious. Mechanistically, bioinformatic analysis demonstrated that LINC01235 inhibited autophagy through sponging miR-224-3p. And miRNA-224-3p targeted RABEP1.ConclusionsLPI promoted endothelial cell activation. LPI induced the expression of LINC01235 and LINC01235 inhibited autophagy through miR-224-3p/RABEP1. Collectively, this study first reveals the function of LINC01235, which may serve as a potential therapeutic target in AS.

33 keywords...

hide…