Association between lncRNA genetic variants and susceptibility to large artery atherosclerotic stroke.

Studies have already illustrated the role of long non-coding RNAs (lncRNAs) in the progression of atherosclerosis, while the potential role of lncRNA gene variation in susceptibility to large artery atherosclerotic stroke (LAAS) remains controversial. We therefore conducted this study to explore and verify the gene expression modules of LAAS. Differentially expressed genes (DEGs) in atherosclerosis were screened in 3 patients with LAAS, and 3 healthy control patients. A further 31 individuals were used to screen DEGs, and MALAT1, MEG3, or SENCR were identified. Real-time PCR and western blotting were used to assess the difference in DEGs between the atherosclerotic and the non-atherosclerotic artery models. A total of 454 DEGs were detected from the initial screening step, and MALAT1, MEG3, or SENCR were applied to predict the risk of LAAS. The AUC of MALAT1, MEG3, and SENCR in predicting the risk of LAAS was 0.746 (95% CI: 0.398-0.753; P = 0.005), 0.575 (95% CI: 0.398-0.753; P = 0.389), and 0.629 (95% CI: 0.449- .808; P = 0.141), respectively. Moreover, there were significant differences between the atherosclerotic and non-atherosclerotic artery models for the expression of MALAT1, GCNT1, VEGFA, and VCAM-1. This study found that the MALAT1 contributes to LAAS susceptibility, and might play an important role in the progression of LAAS.