Long noncoding RNA uc003pxg.1 regulates endothelial cell proliferation and migration via miR‑25‑5p in coronary artery

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Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
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Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

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Ping Li1, Yuan Li2, Lu Chen2

  • 1Department of Central Laboratory, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, Jiangsu 215008, P.R. China.

International Journal of Molecular Medicine
|July 2, 2021
PubMed

Insights

Long noncoding RNA uc003pxg.1 is upregulated in coronary artery disease (CAD). It inhibits human umbilical vein endothelial cell proliferation and migration via microRNA-25-5p, offering insights into CAD mechanisms.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Genetics

Background:

  • Long noncoding RNAs (lncRNAs) are implicated in coronary artery disease (CAD) progression.
  • Previous studies identified uc003pxg.1 upregulation in CAD patients, but its role and mechanism were unknown.

Purpose of the Study:

  • To investigate the expression pattern and biological function of lncRNA uc003pxg.1 in CAD.
  • To elucidate the underlying molecular mechanism of uc003pxg.1 in CAD pathogenesis.

Main Methods:

  • Reverse transcription-quantitative PCR (RT-qPCR) to assess uc003pxg.1 expression in patients with CAD and healthy controls.
  • Small interfering RNA (siRNA) mediated knockdown in human umbilical vein endothelial cells (HUVECs) to evaluate proliferation and migration.
  • Cell Counting Kit-8, cell cycle, EdU, Transwell assays, Western blot, high-throughput sequencing, and dual-luciferase reporter assays were employed.

Main Results:

  • uc003pxg.1 levels were significantly upregulated (~4.6-fold) in 80 CAD patients compared to 80 healthy subjects.
  • Knockdown of uc003pxg.1 inhibited HUVEC proliferation and migration.
  • uc003pxg.1 regulated cyclin D1 and cyclin-dependent kinase expression and targets microRNA-25-5p, mediating its effects on HUVECs.

Conclusions:

  • LncRNA uc003pxg.1 is significantly upregulated in CAD patients.
  • uc003pxg.1 plays a crucial role in regulating endothelial cell function, specifically proliferation and migration, via the miR-25-5p pathway.
  • These findings enhance the understanding of lncRNA uc003pxg.1's role in CAD pathogenesis.

Keywords:
cell proliferation and migrationcoronary artery diseaselong noncoding RNAperipheral blood mononuclear cells

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