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首页> 外文期刊>Circulation journal >Cholesterol effects on endoglin and its downstream pathways in ApoE/LDLR double knockout mice.
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Cholesterol effects on endoglin and its downstream pathways in ApoE/LDLR double knockout mice.

机译：胆固醇对ApoE / LDLR双敲除小鼠中内皮糖蛋白及其下游途径的影响。

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BACKGROUND: The aim of the study was to evaluate whether cholesterol-rich diet affects transforming growth factor-beta-RIII (endoglin) levels in blood and 2 endoglin-related pathways in the aorta of ApoE/LDLR double knockout mice. METHODS AND RESULTS: Mice were fed either chow diet (CHOW) (n=8) or by 1% cholesterol-rich diet (CHOL) (n=8). Biochemical analysis of cholesterol and endoglin levels in blood, lesion size area, immunohistochemistry and Western blot analysis in mice aortas were performed. Biochemical analysis showed that cholesterol-rich diet resulted in a significant increase of cholesterol and endoglin levels in serum, and increased plaque size in the aorta. In addition, a cholesterol-rich diet significantly decreased the expressions of endoglin by 92%, activin receptor-like kinase (ALK)-1 by 71%, p-Smad2 by 21%, and vascular endothelial growth factor (VEGF) by 37% when compared to CHOW mice, but ALK-5, p-Smad1, and endothelial nitric oxide synthase were not significantly affected. CONCLUSIONS: Hypercholesterolemia increases endoglin levels in blood and simultaneously decreases its expression in aorta, together with atherosclerosis protective markers p-Smad2 and VEGF, followed by increased plaque size. Inhibition of endoglin signaling might be one of the mechanisms responsible for the promoting of endothelial dysfunction and atherogenesis. Moreover, the monitoring of endoglin serum levels might represent an attractive blood marker of progression of disease; however, the precise source and role of endoglin in blood serum remains to be elucidated.
机译：背景：这项研究的目的是评估富含胆固醇的饮食是否会影响ApoE / LDLR双敲除小鼠主动脉中血液中的转化生长因子β-RIII（endoglin）水平和2种与内分泌相关的通路。方法和结果：给小鼠饲以低脂饮食（CHOW）（n = 8）或1％高胆固醇饮食（CHOL）（n = 8）。进行了小鼠主动脉中血液中胆固醇和内皮糖蛋白水平的生化分析，病变大小区域，免疫组织化学和蛋白质印迹分析。生化分析表明，高胆固醇饮食会导致血清中胆固醇和内皮糖蛋白水平显着增加，主动脉斑块大小也会增加。此外，富含胆固醇的饮食可显着降低内皮糖蛋白的表达92％，激活素受体样激酶（ALK）-1降低71％，p-Smad2降低21％和血管内皮生长因子（VEGF）降低37％与CHOW小鼠相比，ALK-5，p-Smad1和内皮型一氧化氮合酶没有受到明显影响。结论：高胆固醇血症会增加血液中内皮糖蛋白的水平，并同时降低其在主动脉中的表达，同时还伴有动脉粥样硬化保护标记物p-Smad2和VEGF，随后斑块大小增加。内皮糖蛋白信号的抑制可能是导致内皮功能障碍和动脉粥样硬化发生的机制之一。此外，对内皮糖蛋白血清水平的监测可能代表了疾病进展的有吸引力的血液标志物。然而，内皮糖蛋白在血清中的确切来源和作用仍有待阐明。

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