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dc.creatorKAPLAN,MARIELLE
dc.creatorAVIRAM,MICHAEL
dc.date2004-01-01
dc.date.accessioned2020-02-17T15:34:03Z
dc.date.available2020-02-17T15:34:03Z
dc.identifierhttps://scielo.conicyt.cl/scielo.php?script=sci_arttext&pid=S0716-97602004000200010
dc.identifier.urihttps://revistaschilenas.uchile.cl/handle/2250/131107
dc.descriptionProteoglycans (PGs) from the arterial extracellular matrix (ECM) contribute to the trapping of LDL and oxidized LDL (Ox-LDL) in the arterial wall, a phenomenon called "lipoprotein retention". Moreover, we have shown that subsequent to their binding to the matrix, LDL and Ox-LDL are taken up by macrophages. Oxidative stress significantly increases macrophage secretion of ECM-PGs, lipoprotein binding to the ECM and the uptake of ECM-retained lipoproteins by macrophages. The aim of the present study was to determine whether red wine administration to atherosclerotic mice would affect their peritoneal macrophage-derived extracellular matrix properties, such as the glycosaminoglycan content and the ability to bind LDL. In addition, we questioned the ability of LDL bound to the mice peritoneal macrophages-derived ECM to be taken up by macrophages. Red wine administration to atherosclerotic mice did not affect the mice peritoneal macrophages-derived ECM glycosaminoglycan content but it significantly reduced the mice peritoneal macrophages-derived ECM ability to bind LDL and the subsequent uptake of ECM-retained LDL by the macrophages. The present study thus clearly demonstrated the inhibitory effect of red wine consumption by E0 mice on their peritoneal macrophage-derived extracellular matrix atherogenic properties.
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dc.languageen
dc.publisherSociedad de Biología de Chile
dc.relation10.4067/S0716-97602004000200010
dc.rightsinfo:eu-repo/semantics/openAccess
dc.sourceBiological Research v.37 n.2 2004
dc.subjectAntioxidants
dc.subjectatherosclerosis
dc.subjectextracellular matrix
dc.subjectmacrophages
dc.subjectpolyphenols
dc.subjectproteoglycans
dc.subjectred wine
dc.titleRed Wine administration to Apolipoprotein E-deficient Mice reduces their Macrophage-derived Extracellular Matrix Atherogenic Properties


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