Hsa_ circ_0006867 regulates ox-LDL-induced endothelial injury via the miR-499a-3p/ADAM10 axis

Ji-Ge Hong1,2,3, Hui-Lei Zheng2,3,4, Peng Wang4

  • 1Department of Geriatric Cardiology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.

Insights

Circular RNAs (circRNAs) regulate atherosclerosis by sponging miR-499a-3p, impacting ADAM10. This circ_0006867 pathway offers a potential therapeutic target for endothelial injury.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Genetics

Background:

  • Circular RNAs (circRNAs) are implicated in various disease pathologies.
  • The specific role of circRNAs in atherosclerosis development requires further elucidation.
  • Endothelial dysfunction is a key event in atherosclerosis pathogenesis.

Purpose of the Study:

  • To investigate the mechanism of circRNAs in atherosclerosis.
  • To identify specific circRNAs involved in oxidized low-density lipoprotein (ox-LDL)-induced endothelial injury.
  • To explore the therapeutic potential of identified circRNAs in atherosclerosis.

Main Methods:

  • Human umbilical vein endothelial cells (HUVECs) were treated with ox-LDL to model atherosclerosis.
  • Expression levels of circRNAs were analyzed in treated endothelial cells.
  • The interaction between circ_0006867, miR-499a-3p, and ADAM10 was investigated using molecular assays.

Main Results:

  • Hsa_circ_0006867 (circ_0006867) expression was significantly upregulated in ox-LDL-treated HUVECs.
  • Circ_0006867 functioned as a molecular sponge for miR-499a-3p, regulating its availability.
  • This interaction modulated the expression of the downstream target gene ADAM10, affecting endothelial cell apoptosis and migration.

Conclusions:

  • Circ_0006867 plays a critical role in ox-LDL-induced endothelial injury through the circ_0006867/miR-499a-3p/ADAM10 axis.
  • Circ_0006867 represents a potential therapeutic target for atherosclerosis.
  • Understanding this regulatory axis provides insights into endothelial cell function in cardiovascular disease.