Abstract
Objectives Endothelial cell injury is a critical pathological change during the development of atherosclerosis. Here, we explored the effect of omentin-1 on free fatty acid- (FFA-) induced endothelial cell injury. Methods An FFA-induced endothelial cell injury model was established to investigate the role of omentin-1 in this process. Cell proliferation was analyzed with the Cell Counting Kit assay and flow cytometry. Scratch and transwell assays were used to evaluate cell migration. Factors secreted by endothelial cells after injury were detected by western blotting, reverse-transcription quantitative polymerase chain reaction, and cellular fluorescence assay. Results Omentin-1 rescued the FFA-induced impaired proliferation and migration capabilities of human umbilical vein endothelial cells (HUVECs). It decreased the number of THP-1 cells attached to HUVECs in response to injury and inhibited the FFA-induced proinflammatory state of HUVECs. Conclusion Omentin-1 could partly ameliorate FFA-induced endothelial cell injury.
Highlights
Omentin-1 Reversed the Palmitic acid (PA)-Induced Impairment in the Proliferation and Migration of human umbilical vein endothelial cells (HUVECs). e treatment of HUVECs with PA alone resulted in the inhibition of their proliferation ability as compared with the control and dimethyl sulfoxide (DMSO) treatment (Figure 1(a)). e simultaneous treatment with PA and omentin-1 partly ameliorated the impaired proliferation ability of these cells (Figure 1(a))
Flow cytometry results showed that the proportion of cells in S and G2 phases after treatment with PA alone was lower than that observed after control and DMSO treatment (Figure 1(b)). us, HUVEC division was inhibited by PA
We found that the PA-induced upregulation in the expression of NF-κB was ameliorated by omentin-1 cotreatment (Figure 3(a)), and the PA-induced degradation of IκBα was prevented by omentin1 (Figure 3(a)). us, omentin-1 inhibited the activation of NF-κB
Summary
Endothelial cell injury is a critical pathological change during the development of atherosclerosis. We explored the effect of omentin-1 on free fatty acid- (FFA-) induced endothelial cell injury. An FFA-induced endothelial cell injury model was established to investigate the role of omentin-1 in this process. Factors secreted by endothelial cells after injury were detected by western blotting, reverse-transcription quantitative polymerase chain reaction, and cellular fluorescence assay. Omentin-1 rescued the FFA-induced impaired proliferation and migration capabilities of human umbilical vein endothelial cells (HUVECs). It decreased the number of THP-1 cells attached to HUVECs in response to injury and inhibited the FFA-induced proinflammatory state of HUVECs. Conclusion. Omentin-1 could partly ameliorate FFA-induced endothelial cell injury
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