<p>Endothelial cell damage often results in apoptosis and is thus a crucial factor for the development of coronary artery disease (CAD). However, the mechanisms underlying endothelial cell apoptosis remain unclear. Although circular (circ) RNAs have been implicated in apoptosis, the involvement of hsa_circ_0124644 is uncertain. Therefore, the aim of this study was to investigate the effect of hsa_circ_0124644 on endothelial cell apoptosis and to elucidate the underlying molecular processes. We treated endothelial cells with tumor necrosis factor alpha (TNF-α) to simulate the microenvironment of CAD and generate an apoptosis model. We measured cell apoptosis in conjunction with hsa_circ_0124644 expression. After hsa_circ_0124644 overexpression or inhibition, we assessed apoptosis levels using flow cytometry, RT-qPCR, and western blotting. We found that hsa_circ_0124644 overexpression lowered the apoptosis rate and increased cell viability. Similarly, overexpression also upregulated the expression of an anti-apoptotic protein (Bcl-2) and downregulated that of a pro-apoptotic protein (Bax). In conclusion, our findings suggested that hsa_circ_0124644 mediates endothelial cell apoptosis in CAD. These findings have important implications for developing effective treatments of cardiovascular conditions with excessive apoptosis.</p>

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Circular RNA hsa_circ_0124644 regulates apoptosis of endothelial cells in coronary artery disease

  • Ying Cui,
  • Boxin Zhao,
  • Shimeng Wang,
  • Lin Gui,
  • Yingyu Xiang,
  • Zhiyong Zhang,
  • Xueyuan Sun,
  • Jingyao Fan,
  • Jun Liu,
  • Lijuan Huang

摘要

Endothelial cell damage often results in apoptosis and is thus a crucial factor for the development of coronary artery disease (CAD). However, the mechanisms underlying endothelial cell apoptosis remain unclear. Although circular (circ) RNAs have been implicated in apoptosis, the involvement of hsa_circ_0124644 is uncertain. Therefore, the aim of this study was to investigate the effect of hsa_circ_0124644 on endothelial cell apoptosis and to elucidate the underlying molecular processes. We treated endothelial cells with tumor necrosis factor alpha (TNF-α) to simulate the microenvironment of CAD and generate an apoptosis model. We measured cell apoptosis in conjunction with hsa_circ_0124644 expression. After hsa_circ_0124644 overexpression or inhibition, we assessed apoptosis levels using flow cytometry, RT-qPCR, and western blotting. We found that hsa_circ_0124644 overexpression lowered the apoptosis rate and increased cell viability. Similarly, overexpression also upregulated the expression of an anti-apoptotic protein (Bcl-2) and downregulated that of a pro-apoptotic protein (Bax). In conclusion, our findings suggested that hsa_circ_0124644 mediates endothelial cell apoptosis in CAD. These findings have important implications for developing effective treatments of cardiovascular conditions with excessive apoptosis.