14-3-3-η interacts with BCL-2 to protect human endothelial progenitor cells from ox-LDL-triggered damage

Cell Biol Int. 2024 Mar;48(3):290-299. doi: 10.1002/cbin.12105. Epub 2023 Dec 15.

Abstract

Oxidized low-density lipoprotein (ox-LDL) causes dysfunction of endothelial progenitor cells (EPCs), and we recently reported that 14-3-3-η can attenuate the damage triggered by ox-LDL in EPCs. However, the molecular mechanisms by which 14-3-3-η protects EPCs from the damage caused by ox-LDL are not fully understood. In this study, we observed that the expression of 14-3-3-η and BCL-2 were downregulated in ox-LDL-treated EPCs. Overexpression of 14-3-3-η in ox-LDL-treated EPC significantly increased BCL-2 level, while knockdown of BCL-2 reduced 14-3-3-η expression and mitigated the protective effect of 14-3-3-η on EPCs. In addition, we discovered that 14-3-3-η colocalizes and interacts with BCL-2 in EPCs. Taken together, these data suggest that 14-3-3-η protects EPCs from ox-LDL-induced damage by its interaction with BCL-2.

Keywords: 14-3-3-η; BCL-2; apoptosis; endothelial progenitor cells; oxidized low-density lipoprotein (ox-LDL).

MeSH terms

  • Apoptosis
  • Cells, Cultured
  • Endothelial Progenitor Cells* / metabolism
  • Human Umbilical Vein Endothelial Cells / metabolism
  • Humans
  • Lipoproteins, LDL / metabolism
  • Lipoproteins, LDL / pharmacology
  • Proto-Oncogene Proteins c-bcl-2 / metabolism

Substances

  • BCL2 protein, human
  • Lipoproteins, LDL
  • oxidized low density lipoprotein
  • Proto-Oncogene Proteins c-bcl-2
  • YWHAH protein, human