Cholesterol Effects on Endoglin and Its Downstream Pathways in ApoE/LDLR Double Knockout Mice

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  • Strasky Zbynek
    Department of Biological and Medical Sciences, Faculty of Pharmacy in Hradec Kralove, Charles University in Prague
  • Vecerova Lenka
    Department of Biological and Medical Sciences, Faculty of Pharmacy in Hradec Kralove, Charles University in Prague
  • Rathouska Jana
    Department of Biological and Medical Sciences, Faculty of Pharmacy in Hradec Kralove, Charles University in Prague
  • Slanarova Martina
    Department of Biological and Medical Sciences, Faculty of Pharmacy in Hradec Kralove, Charles University in Prague
  • Brcakova Eva
    Department of Biological and Medical Sciences, Faculty of Pharmacy in Hradec Kralove, Charles University in Prague
  • Kudlackova Zdenka
    Department of Biological and Medical Sciences, Faculty of Pharmacy in Hradec Kralove, Charles University in Prague
  • Andrys Ctirad
    Institute of Clinical Immunology and Allergology, University Hospital Hradec Kralove
  • Micuda Stanislav
    Department of Pharmacology, Faculty of Medicine in Hradec Kralove, Charles University in Prague
  • Nachtigal Petr
    Department of Biological and Medical Sciences, Faculty of Pharmacy in Hradec Kralove, Charles University in Prague

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Background: The aim of the study was to evaluate whether cholesterol-rich diet affects transforming growth factor-β-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. (Circ J 2011; 75: 1747-1755)<br>

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  • Circulation Journal

    Circulation Journal 75 (7), 1747-1755, 2011

    一般社団法人 日本循環器学会

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