The Clinical Value of LINC01094/Hsa-miR-4758-5p and Their Action Mechanisms in Carotid Artery Stenosis.

Abstract

Carotid artery stenosis (CAS) is mostly caused by carotid atherosclerotic plaque, leading to various cardiovascular and cerebrovascular diseases that seriously threaten human lives. This study aims to explore the roles of LINC01094 and hsa-miR-4758-5p in CAS pathogenesis and provide theoretical support for its prediction and treatment. RT-qPCR was used to detect the levels of LINC01094 and hsa-miR-4758-5p. SPSS software was utilized to construct the Receiver Operating Characteristic (ROC) curves for diagnosingCAS using LINC01094 and hsa-miR-4758-5p. The interaction between LINC01094 and hsa-miR-4758-5p was tested using a dual-luciferase reporter gene assay. CCK-8 assay and flow cytometry were employed to assess cell activity and apoptotic cell ratio, respectively. The Western Blotting assay detected the expression of BAK, BCL-2, and ICAM-1. ELISA, lipid peroxidation (MDA), and reactive oxygen species (ROS) kits measured the levels of inflammatory factors (IL-6 and TNF-α), MDA, and ROS, respectively. LINC01094 expressed highly, and hsa-miR-4758-5p expressed lowly in CAS. The combination of LINC01094 and hsa-miR-4758-5p showed higher accuracy in diagnosing CAS compared to either factor alone. The hsa-miR-4758-5p mimic significantly reduced the luciferase activity of HCAECs and THP-1 cells transfected with wt-LINC01094 vectors. LINC01094 overexpression suppressed the level of hsa-miR-4758-5p. The hsa-miR-4758-5p mimic reversed cell damage induced by ox-LDL or LINC01094 overexpression. LINC01094 and hsa-miR-4758-5p had good diagnostic value in CAS. Mechanistically, LINC01094 mediated ox-LDL-induced damage of HCAECs and THP-1 cells by negatively regulating hsa-miR-4758-5p.