| First Author | Liu H | Year | 2019 |
| Journal | Biomed Res Int | Volume | 2019 |
| Pages | 7157865 | PubMed ID | 31781638 |
| Mgi Jnum | J:292503 | Mgi Id | MGI:6448728 |
| Doi | 10.1155/2019/7157865 | Citation | Liu H, et al. (2019) Adipokine Chemerin Stimulates Progression of Atherosclerosis in ApoE(-/-) Mice. Biomed Res Int 2019:7157865 |
| abstractText | Background: Vascular remodeling is the most critical pathogenesis of atherosclerosis. Adipokine chemerin was known for its relationship with obesity as well as metabolism. Most recently, chemerin was found to play a crucial role in the pathologic process of cardiovascular diseases including coronary heart disease. In this study, we surveyed the role of chemerin in progression of atherosclerosis in ApoE(-/-) mice. Objective: To investigate the relationship between chemerin and progression of atherosclerosis in ApoE(-/-) mice and its mechanism. Methods: 8-week-old ApoE(-/-) mice were fed with high-fat diet to induce the atherosclerosis model. Adenoviruses were transfected for knockdown or overexpression of chemerin gene into aorta. Serums and aortic tissues of ApoE(-/-) mice were obtained after feeding high-fat diet for 16 weeks. HE staining and oil red staining were performed to evaluate aortic plaque. ELISA was performed to explore serum levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and transforming growth factor-beta1 (TGF-beta1). Real-time PCR and western blotting were carried out to investigate the mRNA and protein levels of chemerin, nuclear factor-kappaB p65 (NF-kappaBp65), proliferating cell nuclear antigen (PCNA), phosphorylated p38 mitogen-activated protein kinase (p-p38-MAPK), phosphorylated c-Jun N-terminal kinase (p-JNK), and phosphorylated extracellular signal regulated kinase 1/2 (p-ERK 1/2). Result: Aortic plaque formation was significantly induced by high-fat diet in ApoE(-/-) mice. Simultaneously, elevated serum levels of TNF-alpha and IL-1beta and elevated mRNA and protein levels of chemerin, NF-kappaBp65, PCNA, p-p38-MAPK, p-JNK, and p-ERK 1/2 were found in ApoE(-/-) mice. After aortic chemerin gene was inhibited by adenovirus, aortic atherosclerosis induced by high-fat diet was significantly meliorated, serum levels of TNF-alpha and IL-1beta decreased, mRNA and protein levels of NF-kappaBp65, PCNA, p-p38-MAPK, p-JNK, and p-ERK 1/2 decreased simultaneously. Conclusion: Our study revealed that chemerin stimulated the progression of atherosclerosis in ApoE(-/-) mice. |
