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

Shu-Xin Zhang, Cheng-Hong Yu

The Kaohsiung journal of medical sciences 2023 Jan

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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. © 2022 The Authors. The Kaohsiung Journal of Medical Sciences published by John Wiley & Sons Australia, Ltd on behalf of Kaohsiung Medical University.

Citation

Shu-Xin Zhang, Cheng-Hong Yu. Silencing of UCA1 attenuates the ox-LDL-induced injury of human umbilical vein endothelial cells via miR-873-5p/MAPK8 axis. The Kaohsiung journal of medical sciences. 2023 Jan;39(1):6-15