AIBP reduces atherosclerosis by promoting reverse cholesterol transport and ameliorating inflammation in apoE −/− mice
Autor: | Feng Yao, Zhen-Wang Zhao, Xiao-Er Tang, Ling-Yan Chen, Xiao-Dan Xia, Xi-Long Zheng, Min Zhang, Chao-Ke Tang, Duo Gong, Guo-Jun Zhao |
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Rok vydání: | 2018 |
Předmět: |
Male
0301 basic medicine medicine.medical_specialty Inflammation 030204 cardiovascular system & hematology Mice 03 medical and health sciences chemistry.chemical_compound Apolipoproteins E 0302 clinical medicine Internal medicine medicine Animals Macrophage chemistry.chemical_classification biology Cholesterol Binding protein Reverse cholesterol transport Biological Transport NF-κB Atherosclerosis Amino acid DNA-Binding Proteins 030104 developmental biology Endocrinology chemistry ABCA1 biology.protein lipids (amino acids peptides and proteins) medicine.symptom Cardiology and Cardiovascular Medicine |
Zdroj: | Atherosclerosis. 273:122-130 |
ISSN: | 0021-9150 |
DOI: | 10.1016/j.atherosclerosis.2018.03.010 |
Popis: | Background and aims ApoA-1 binding protein (AIBP) is a secreted protein that interacts with apoA-I and accelerates cholesterol efflux from cells. We have recently reported that AIBP promotes apoA-1 binding to ABCA1 in the macrophage cell membrane, partially through 115–123 amino acids. However, the effects of AIBP on the development of atherosclerosis in vivo remain unknown. Methods ApoE−/− mice with established atherosclerotic plaques were infected with rAAV-AIBP or rAAV-AIBP(Δ115-123), respectively. Results AIBP-treated mice showed reduction of atherosclerotic lesion formation, increase in circulating HDL levels and enhancement of reverse cholesterol transport to the plasma, liver, and feces. AIBP increased ABCA1 protein levels in aorta and peritoneal macrophages. Furthermore, AIBP could diminish atherosclerotic plaque macrophage content and the expression of chemotaxis-related factors. In addition, AIBP prevented macrophage inflammation by inactivating NF-κB and promoted the expression of M2 markers like Mrc-1 and Arg-1. However, lack of 115–123 amino acids of AIBP(Δ115-123) had no such preventive effects on the progression of atherosclerosis. Conclusions Our observations demonstrate that AIBP inhibits atherosclerosis progression and suggest that it may be an effective target for prevention of atherosclerosis. |
Databáze: | OpenAIRE |
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