LINC01094 exacerbates acute cerebral infarction by regulating miR-499a-5p

The purpose of this study is to clarify the role of LINC01094 in acute cerebral infarction (ACI) and to explore its potential molecular mechanisms. A total of 121 patients with ACI and 133 healthy controls were enrolled in this study. The expression levels of LINC01094, miR-499a-5p, and inflammatory markers (CRP, IL-6) were measured using RT-qPCR. The levels of MDA, SOD, and ROS were measured using commercial assay kits. The diagnostic value of LINC01094 for ACI was evaluated using ROC curve analysis. CCK-8 assay and flow cytometry were utilized to measure cell viability and apoptosis. The subcellular localization of LINC01094 in SH-SY5Y cells was determined. The predicted targeting relationship between LINC01094 and miR-499a-5p was validated using dual-luciferase reporter (DLR) and RNA immunoprecipitation (RIP) assays. Serum LINC01094 expression was significantly elevated in ACI patients and demonstrated diagnostic value for ACI. miR-499a-5p expression was markedly reduced in both ACI patients and in vitro/in vivo models, showing a significant negative correlation with LINC01094 expression in patients. Downregulation LINC01094 mitigated OGD/R-induced damage in SH-SY5Y cells and cerebral injury in MCAO rats, while inhibition miR-499a-5p reversed this protective effect. Furthermore, CACNB2 was confirmed as a direct target of miR-499a-5p. LINC01094 participates in the pathological process of ACI injury by competitively binding to and inhibiting the activity of miR-499a-5p. These findings suggest that LINC01094 may serve as a potential therapeutic target for ACI treatment.