Abstract
BackgroundAtherosclerosis (AS) is a chronic and progressive disease primarily induced by inflammation of the arterial blood vessel wall. Investigating the function and molecular regulation mechanisms of ET-1, ERβ, and FOXN1 in disease models will provide new targets and means for clinical treatment.MethodsThe effects of ET-1 on oxidative stress in HUVEC were verified through quantitative polymerase chain reaction (qPCR), western blot, flow cytometry, as well as dual luciferase reporter gene and biochemical assays.ResultsCompared with the ET-1+ negative control (NC) group, the ERβ messenger ribonucleic acid (mRNA) expression level was significantly reduced, and the FOXN1 mRNA expression level increased markedly in the ET-1 + ERβ small interfering ribonucleic acid (siRNA) group. Meanwhile, the FOXN1 mRNA expression level was significantly reduced in the ET-1 + FOXN1 siRNA group. FOXN1 promoter luciferase reporter gene activity was notably enhanced in the ERβ siRNA group compared with the siRNA control group. Compared with the ET-1 + NC group, the levels of reaction oxygen species (ROS) in the ET-1 + ERβ siRNA group increased considerably, the superoxide dismutase (SOD) level was significantly reduced, and the G0/G1 phase cell ratio was reduced. In addition, the protein expression of ERβ and cyclin B1 (CCNB1) was markedly reduced, whereas the protein expression of cyclin A2 (CCNA2), cyclin D1 (CCND1), and cyclin E1 (CCNE1) increased substantially. The opposite result was observed in the ET-1 + FOXN1 siRNA group.ConclusionsET-1 can contribute to the expression of ERβ and FOXN1. ERβ can inhibit the expression of FOXN1 by regulating promoter activity. The ET-1/ERβ/FOXN1 signaling pathway is involved in the regulation of oxidative stress and cycle progression in HUVEC. This study provides a new mechanism for the regulation of umbilical vein endothelial cells. The ET-1/ERβ/FOXN1 signaling pathway may provide novel therapeutic targets and strategies for the treatment of atherosclerosis.
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