Adipokine Chemerin Stimulates Progression of Atherosclerosis in ApoE−/− Mice

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...

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Main Authors: Huadong Liu, Wei Xiong, Yu Luo, Hua Chen, Yaqiong He, Yuanzhi Cao, Shaohong Dong
Format: Article
Language:English
Published: Hindawi Limited 2019-01-01
Series:BioMed Research International
Online Access:http://dx.doi.org/10.1155/2019/7157865
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spelling doaj-5d8cfae8e8954ea8a736f0c8700b706c2020-11-25T02:31:04ZengHindawi LimitedBioMed Research International2314-61332314-61412019-01-01201910.1155/2019/71578657157865Adipokine Chemerin Stimulates Progression of Atherosclerosis in ApoE−/− MiceHuadong Liu0Wei Xiong1Yu Luo2Hua Chen3Yaqiong He4Yuanzhi Cao5Shaohong Dong6Department of Cardiology, Shenzhen People’s Hospital, The Second Affiliated Hospital of Jinan Medical College, Shenzhen 518020, ChinaDepartment of Cardiology, Shenzhen People’s Hospital, The Second Affiliated Hospital of Jinan Medical College, Shenzhen 518020, ChinaDepartment of Gerontology, Shenzhen People’s Hospital, The Second Affiliated Hospital of Jinan Medical College, Shenzhen 518020, ChinaDepartment of Emergency, Shenzhen People’s Hospital, The Second Affiliated Hospital of Jinan Medical College, Shenzhen 518020, ChinaDepartment of Cardiology, Shenzhen People’s Hospital, The Second Affiliated Hospital of Jinan Medical College, Shenzhen 518020, ChinaDepartment of Cardiology, Shenzhen People’s Hospital, The Second Affiliated Hospital of Jinan Medical College, Shenzhen 518020, ChinaDepartment of Cardiology, Shenzhen People’s Hospital, The Second Affiliated Hospital of Jinan Medical College, Shenzhen 518020, ChinaBackground. 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-α (TNF-α), interleukin-1β (IL-1β), and transforming growth factor-β1 (TGF-β1). Real-time PCR and western blotting were carried out to investigate the mRNA and protein levels of chemerin, nuclear factor-κB p65 (NF-κBp65), 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-α and IL-1β and elevated mRNA and protein levels of chemerin, NF-κBp65, 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-α and IL-1β decreased, mRNA and protein levels of NF-κBp65, 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.http://dx.doi.org/10.1155/2019/7157865
collection DOAJ
language English
format Article
sources DOAJ
author Huadong Liu
Wei Xiong
Yu Luo
Hua Chen
Yaqiong He
Yuanzhi Cao
Shaohong Dong
spellingShingle Huadong Liu
Wei Xiong
Yu Luo
Hua Chen
Yaqiong He
Yuanzhi Cao
Shaohong Dong
Adipokine Chemerin Stimulates Progression of Atherosclerosis in ApoE−/− Mice
BioMed Research International
author_facet Huadong Liu
Wei Xiong
Yu Luo
Hua Chen
Yaqiong He
Yuanzhi Cao
Shaohong Dong
author_sort Huadong Liu
title Adipokine Chemerin Stimulates Progression of Atherosclerosis in ApoE−/− Mice
title_short Adipokine Chemerin Stimulates Progression of Atherosclerosis in ApoE−/− Mice
title_full Adipokine Chemerin Stimulates Progression of Atherosclerosis in ApoE−/− Mice
title_fullStr Adipokine Chemerin Stimulates Progression of Atherosclerosis in ApoE−/− Mice
title_full_unstemmed Adipokine Chemerin Stimulates Progression of Atherosclerosis in ApoE−/− Mice
title_sort adipokine chemerin stimulates progression of atherosclerosis in apoe−/− mice
publisher Hindawi Limited
series BioMed Research International
issn 2314-6133
2314-6141
publishDate 2019-01-01
description 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-α (TNF-α), interleukin-1β (IL-1β), and transforming growth factor-β1 (TGF-β1). Real-time PCR and western blotting were carried out to investigate the mRNA and protein levels of chemerin, nuclear factor-κB p65 (NF-κBp65), 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-α and IL-1β and elevated mRNA and protein levels of chemerin, NF-κBp65, 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-α and IL-1β decreased, mRNA and protein levels of NF-κBp65, 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.
url http://dx.doi.org/10.1155/2019/7157865
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