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

Abstract

AbstractOxidized 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.