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THRIL mediates endothelial progenitor cells autophagy via AKT pathway and FUS

Jiandong Xiao1,2, Yuli Lu3, Xinchun Yang4

  • 1Department of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, No.8 Gongren Tiyuchang Nanlu, Chaoyang District, Beijing, 100020, China.

Molecular Medicine (Cambridge, Mass.)
|September 10, 2020
PubMed

Insights

Long non-coding RNA THRIL promotes coronary atherosclerotic heart disease (CAD) by inhibiting endothelial progenitor cell proliferation and mediating autophagy via the AKT pathway and FUS protein.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research

Background:

  • Coronary atherosclerotic heart disease (CAD) is a significant health concern.
  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cardiovascular diseases.

Purpose of the Study:

  • To investigate the role of lncRNA THRIL in CAD.
  • To elucidate the mechanisms by which THRIL affects endothelial progenitor cells (EPCs), including its regulation of the AKT signaling pathway and interaction with FUS protein.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) to measure THRIL expression in CAD blood samples and EPCs.
  • Assays to assess EPC autophagy, viability, and apoptosis.
  • Western blotting to detect protein expression.
  • RNA electrophoretic mobility shift assay (RNA EMSA) and RNA immunoprecipitation (RIP) to confirm interactions between THRIL and FUS.

Main Results:

  • THRIL expression was upregulated in CAD patients and EPCs.
  • Knockdown of THRIL enhanced EPC viability, inhibited autophagy, and suppressed CAD development.
  • THRIL interacted with FUS protein, influencing cell proliferation, autophagy, and the AKT pathway.

Conclusions:

  • THRIL plays a detrimental role in CAD progression.
  • THRIL inhibits EPC proliferation and mediates autophagy through the AKT pathway and FUS interaction.
Abstract

Keywords:
AKTCoronary heart diseaseFUSTHRIL

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