Abstract
BackgroundThe role of adipokines in the development of atherosclerosis (AS) has received increasing attention in recent years. This study aimed to explore the effects of chemerin on the functions of human endothelial progenitor cells (EPCs) and to investigate its role in lipid accumulation in ApoE-knockout (ApoE−/−) mice.MethodsEPCs were cultured and treated with chemerin together with the specific p38 mitogen-activated protein kinase (MAPK) inhibitor SB 203580 in a time- and dose-dependent manner. Changes in migration, adhesion, proliferation and the apoptosis rate of EPCs were detected. ApoE−/− mice with high-fat diet-induced AS were treated with chemerin with or without SB 203580. Weights were recorded, lipid indicators were detected, and tissues sections were stained.ResultsThe data showed that chemerin enhanced the adhesion and migration abilities of EPCs, and reduced the apoptosis ratio and that this effect might be mediated through the p38 MAPK pathway. Additionally, chemerin increased the instability of plaques. Compared with the control group and the inhibitor group, ApoE−/− mice treated with chemerin protein had more serious arterial stenosis, higher lipid contents in plaques and decreased collagen. Lipid accumulation in the liver and kidney and inflammation in the hepatic portal area were enhanced by treatment with chemerin, and the size of adipocytes also increased after chemerin treatment. In conclusion, chemerin can enhance the adhesion and migration abilities of human EPCs and reduce the apoptosis ratio. In animals, chemerin can increase lipid accumulation in atherosclerotic plaques and exacerbate plaques instability. At the same time, chemerin can cause abnormal lipid accumulation in the livers and kidneys of model animals. After specifically blocking the p38 MAPK pathway, the effect of chemerin was reduced.ConclusionsIn conclusion, this study showed that chemerin enhances the adhesion and migration abilities of EPCs and increases the instability of plaques and abnormal lipid accumulation in ApoE−/− mice. Furthermore, these effects might be mediated through the p38 MAPK pathway.
Highlights
The role of adipokines in the development of atherosclerosis (AS) has received increasing attention in recent years
In conclusion, this study showed that chemerin enhances the adhesion and migration abilities of endothelial progenitor cells (EPCs) and increases the instability of plaques and abnormal lipid accumulation in ApoE−/− mice
These effects might be mediated through the p38 mitogen-activated protein kinase (MAPK) pathway
Summary
The role of adipokines in the development of atherosclerosis (AS) has received increasing attention in recent years. Several studies have indicated that lipid metabolism dysfunction and inflammation dominate in the pathological process of AS and that the interaction between these processes promotes AS progression [1,2,3]. Adipocytokines secreted by adipocytes play a critical role in lipid metabolism and inflammation, which are emerging targets in AS and related diseases [5,6,7]. Representative adipocytokines, such as hypersensitive C-reactive protein (hsCRP), leptin, adiponectin and tumour necrosis factor-α (TNF-α), participate in AS by affecting the brain, the liver, skeletal muscle, islets, gonads, immune organs and the vasculature in a systematic manner [8,9,10]
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