Circular RNA Circ-BANP Regulates Oxidized Low-density Lipoprotein-induced Endothelial Cell Injury Through Targeting

Guang Chen1, Yongjun Li2, Ailing Zhang3

  • 1Department of Cardiology, 920 Hospital of Joint Longistics Support Force of Chinese People's Liberation Army, Kunming, China.

Insights

Circular RNA BTG3-associated nuclear protein (circ-BANP) exacerbates endothelial cell dysfunction in atherosclerosis. Inhibiting circ-BANP protects against oxidized LDL-induced injury by targeting the miR-370/TXNIP axis.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Cell Biology

Background:

  • Endothelial cell dysfunction is a key factor in atherosclerosis (AS) pathogenesis.
  • Circular RNAs (circRNAs) play a role in AS development.
  • circRNA BTG3-associated nuclear protein (circ-BANP) involvement in endothelial dysfunction is unclear.

Purpose of the Study:

  • To investigate the role of circ-BANP in oxidized low-density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cell (HUVEC) dysfunction.
  • To elucidate the underlying molecular mechanism involving miR-370 and thioredoxin-interacting protein (TXNIP).

Main Methods:

  • Quantitative real-time PCR and Western blot to measure circ-BANP, miR-370, and TXNIP levels.
  • Cellular assays (viability, apoptosis, migration, invasion, tube formation) to assess HUVEC function.
  • Dual-luciferase reporter assay to confirm targeting interactions.

Main Results:

  • circ-BANP was upregulated in AS blood and ox-LDL-treated HUVECs.
  • circ-BANP inhibition improved HUVEC viability, migration, invasion, tube formation, and reduced apoptosis and inflammation.
  • circ-BANP directly targeted miR-370, which in turn targeted TXNIP, mediating the effects on HUVEC injury.

Conclusions:

  • circ-BANP promotes ox-LDL-induced HUVEC injury via the miR-370/TXNIP pathway.
  • circ-BANP acts as a potential therapeutic target for AS.

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