Overexpression of microRNA-155 alleviates palmitate-induced vascular endothelial cell injury in human umbilical vein endothelial cells by negatively regulating the Wnt signaling pathway

The present study aimed to investigate the effect of microRNA155 (miR-155) on palmitate-induced vascular endothelial cell injury in human umbilical vein endothelial cells (HUVECs) via the regulation of the Wnt signaling pathway. HUVECs were treated with 0.1 mM palmitate. After transfection with mimic, antagomir or the Wnt pathway inhibitor XAV939, HUVECs were divided into six treatment groups: Control, palmitate, mimic + palmitate, mimic + palmitate + XAV939, antagomir + palmitate, antagomir + palmitate + XAV939. miR-155 expression was detected using reverse transcription-quantitative PCR. The expression levels of the Wnt signaling pathway-related factors β-catenin and Cyclin D, and the inflammatory factors interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), were detected using western blot analysis. MTT and Transwell assays were used to detect the proliferation and migration of cells, respectively. Apoptosis and reactive oxygen species (ROS) levels were determined using flow cytometry. The localization of β-catenin in cells was determined by immunofluorescence. Palmitate reduced the expression level of miR-155 in HUVECs. In palmitate-induced HUVECs, overexpression of miR-155 promoted cell proliferation, reduced the levels of apoptosis, downregulated IL-6 and TNF-α expression, and reduced ROS levels. Inhibition of the Wnt signaling pathway enhanced the anti-endothelial cell injury effect caused by the overexpression of miR-155 in palmitate-induced HUVECs, thereby promoting proliferation, reducing apoptosis, downregulating the levels of inflammatory factors and reducing ROS levels. In summary, overexpression of miR-155 inhibited palmitate-induced apoptosis, ROS production and levels of inflammatory factors, and promoted the proliferation of HUVECs by negatively regulating the Wnt signaling pathway. This present study provides a theoretical basis for the prevention and treatment of cardiovascular diseases associated with endothelial cell injury.