LncRNA THRIL Functions as a Marker for Carotid Artery Stenosis and Affects the Biological Function of Human Aortic Endothelial Cell
- PMID: 37313306
- PMCID: PMC10259528
- DOI: 10.2147/JIR.S409679
LncRNA THRIL Functions as a Marker for Carotid Artery Stenosis and Affects the Biological Function of Human Aortic Endothelial Cell
Abstract
Purpose: Carotid artery restenosis (CAS) is a leading contributor to cerebrovascular diseases and one of the leading causes of death in the world. The purpose of this study was to assess the predictive efficiency of long non-coding RNA (lncRNA) TNFalpha-and hnRNP L-related immunoregulatory lncRNA (THRIL) and its association with the pathogenesis of CAS.
Patients and methods: The expression of THRIL was determined in patients with asymptomatic CAS and human aortic endothelial cell (HAEC) models induced by oxidized low-density lipoprotein (ox-LDL). The receiver operating characteristic (ROC) curve and Kaplan-Meier (K-M) drawings were constructed to predict the risk of poor prognosis in patients with CAS. The cell proliferation, death rate, and inflammation were detected by 3-(4,5-dimethyl-2-thiazyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT), flow cytometry, and enzyme-linked immunosorbent assay (ELISA) assays.
Results: The relative expression of THRIL was elevated in patients with asymptomatic CAS. The findings of ROC curve indicated that THRIL had a predictive possibility on CAS. K-M finding and Cox regression analysis showed that the expression of THRIL and the degree of CAS were independent risk factors for poor prognosis in patients with CAS. THRIL was up-expressed in HAECs induced by ox-LDL. Down-regulation of THRIL could promote the proliferation of HAECs, inhibit cell apoptosis, and restrict cell inflammation.
Conclusion: THRIL was a diagnostic and prognostic biomarker in CAS and played an important role in regulating the proliferation, apoptosis, and inflammation of HAECs induced by ox-LDL.
Keywords: THRIL; carotid artery restenosis; diagnosis; prognosis; proliferation.
© 2023 Wang et al.
Conflict of interest statement
The authors report no conflicts of interest in this work.
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