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- W2126706148 abstract "Objective— To determine the role of monocyte chemoattractant protein-1 (Mcp-1) on the progression of visceral fat-induced atherosclerosis. Methods and Results— Visceral fat inflammation was induced by transplantation of perigonadal fat. To determine whether recipient Mcp-1 status affected atherosclerosis induced by inflammatory fat, apolipoprotein E-deficient ( ApoE −/− ) and ApoE −/− and Mcp-1-deficient ( Mcp-1 −/− ) mice underwent visceral fat transplantation. Intravital microscopy was used to study leukocyte-endothelial interactions. To study the primary tissue source of circulating Mcp-1, both fat and bone marrow transplantation experiments were used. Transplantation of visceral fat increased atherosclerosis in ApoE −/− mice but had no effect on atherosclerosis in ApoE −/− , Mcp-1 −/− mice. Intravital microscopy revealed increased leukocyte attachment to the endothelium in ApoE −/− mice compared with ApoE −/− , Mcp-1 −/− mice after receiving visceral fat transplants. Transplantation of visceral fat increased plasma Mcp-1, although donor adipocytes were not the source of circulating Mcp-1 because no Mcp-1 was detected in plasma from ApoE −/− , Mcp-1 −/− mice transplanted with Wt fat, indicating that recipient Mcp-1-producing cells were affecting the atherogenic response to the fat transplantation. Consistently, transplantation of Mcp-1 −/− fat to ApoE −/− mice did not lead to atheroprotection in recipient mice. Bone marrow transplantation between Wt and Mcp-1 −/− mice indicated that the primary tissue source of circulating Mcp-1 was the endothelium. Conclusion— Recipient Mcp-1 deficiency protects against atherosclerosis induced by transplanted visceral adipose tissue." @default.
- W2126706148 created "2016-06-24" @default.
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- W2126706148 date "2010-06-01" @default.
- W2126706148 modified "2023-09-27" @default.
- W2126706148 title "Monocyte Chemoattractant Protein-1 Deficiency Protects Against Visceral Fat-Induced Atherosclerosis" @default.
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- W2126706148 doi "https://doi.org/10.1161/atvbaha.110.205914" @default.
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