Silencing of UCA1 attenuates the ox‐LDL‐induced injury of human umbilical vein endothelial cells via miR‐873‐5p/MAPK8 axis

Abstract

Abstract LncRNA UCA1 plays a vital role in cardiovascular diseases. Endothelial cell dysfunction is a prerequisite for atherosclerosis (AS) development. However, the pathophysiological role of UCA1 in endothelial cell dysfunction induced by ox‐LDL remains obscure. Here, we observed that UCA1 was upregulated in the sera of patients with AS and ox‐LDL‐treated endothelial cells. UCA1 knockdown dramatically reduced the cell apoptosis induced by ox‐LDL and the production of pro‐inflammatory cytokines and ROS in endothelial cells. Mechanistically, we found that UCA1 directly targeted miR‐873‐5p. UCA1 knockdown increased, while UCA1 overexpression decreased the expression of miR‐873‐5p. Further, we found that mitogen‐activated protein kinase 8 (MAPK8) was a downstream target gene of miR‐873‐5p. MAPK8 overexpression or miR‐873‐5p knockdown reduced the enhancement of ox‐LDL‐induced cell apoptosis, oxidative stress, and pro‐inflammatory cytokine production conferred by UCA1 knockdown. In conclusion, UCA1 can protect Human Umbilical Vein Endothelial Cells from ox‐LDL‐induced injury via the miR‐873‐5p/MAPK8 axis.