Objective Type 1 myocardial infarction (T1MI) is primarily caused by the formation of coronary thrombi, which leads to acute myocardial ischemia and hypoxia and is associated with high morbidity and mortality rates. However, the effects of thrombus-derived exosomes (TEs) on endothelial cell function remain unclear. The aim of this study was to investigate the interaction between lncRNA LOC101928697, which is enriched in TEs, and FUS proteins, as well as their impact on endothelial cell function. Methods Thrombus-derived exosomes were extracted from thrombi collected from patients with T1MI, and lncRNAs with differential expression were identified through microarray analysis. Bioinformatic analyses were used to predict the interaction between LOC101928697 and FUS protein. The effects of TEs and LOC101928697 on human umbilical vein endothelial cells (HUVECs) were evaluated using CCK8 assays, scratch assays, cell cycle analysis, fluorescence in situ hybridization, and RT-PCR. The role of LOC101928697 was further confirmed by knockdown experiments. Results Our study indicates that TEs exert a significant inhibitory effect on the proliferation and migration of HUVECs, and that this effect is mediated by LOC101928697. LOC101928697 is highly enriched in TEs and has been shown to regulate the expression levels of CyclinD1 and PCNA by binding to FUS proteins, thereby inhibiting the proliferative capacity of endothelial cells. Furthermore, the inhibition of HUVEC proliferation and migration induced by TEs was significantly ameliorated by knockdown of LOC101928697. Conclusion This study provides new insights into the mechanism by which TEs suppress endothelial cell function via the LOC101928697-FUS axis. These findings highlight a molecular target that may contribute to the progression of T1MI and provide a foundation for future research into diagnostic and therapeutic strategies for cardiovascular diseases.
He et al. (Tue,) studied this question.