LncRNA THRIL Functions as a Marker for Carotid Artery Stenosis and Affects the Biological Function of Human Aortic

Fei Wang1, Ying Wang2, Xichun Guo3

  • 1Department of Neurosurgery, Affiliated Hospital of Weifang Medical University, Weifang, People's Republic of China.

Insights

Long non-coding RNA THRIL is elevated in carotid artery restenosis (CAS) and predicts poor prognosis. Down-regulating THRIL impacts endothelial cell proliferation, apoptosis, and inflammation, suggesting its role in CAS pathogenesis.

Area of Science:

  • Vascular Biology
  • Molecular Medicine
  • Biomarker Discovery

Background:

  • Carotid artery restenosis (CAS) is a significant cause of cerebrovascular disease and mortality.
  • Understanding the molecular mechanisms underlying CAS is crucial for developing effective diagnostic and therapeutic strategies.

Purpose of the Study:

  • To evaluate the predictive value of long non-coding RNA (lncRNA) TNFalpha-and hnRNP L-related immunoregulatory lncRNA (THRIL) in CAS.
  • To investigate the association of THRIL with the pathogenesis of CAS.

Main Methods:

  • THRIL expression was measured in patients with asymptomatic CAS and in human aortic endothelial cells (HAECs) exposed to oxidized low-density lipoprotein (ox-LDL).
  • Receiver operating characteristic (ROC) curves and Kaplan-Meier (K-M) analysis were used for prognosis prediction.
  • Cell proliferation, apoptosis, and inflammation were assessed using MTT, flow cytometry, and ELISA.

Main Results:

  • THRIL expression was significantly higher in patients with CAS.
  • ROC analysis confirmed THRIL's predictive potential for CAS.
  • K-M and Cox regression revealed THRIL expression and CAS severity as independent risk factors for poor prognosis.
  • THRIL was upregulated in ox-LDL-induced HAECs, and its downregulation promoted proliferation, inhibited apoptosis, and reduced inflammation.

Conclusions:

  • THRIL serves as a diagnostic and prognostic biomarker for CAS.
  • THRIL plays a critical role in regulating endothelial cell behavior, including proliferation, apoptosis, and inflammation, in the context of ox-LDL exposure.
Abstract

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