Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
Schuler-Lüttmann, S; Zhu, Y; Hoffmann, M; März, W; Feussner, G; Wieland, H; Assmann, G; von Eckardstein, A.
Cholesterol efflux from normal and Tangier disease fibroblasts into normal, high-density lipoprotein-deficient, and apolipoprotein E-deficient plasmas.
Metabolism. 2000; 49(6):770-777
Doi: 10.1053/meta.2000.6243
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- Co-Autor*innen der Med Uni Graz
- März Winfried
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- Abstract:
- Tangier disease (TD) fibroblasts have defective cholesterol release in the presence of lipid-free apolipoproteins. We compared normolipidemic probands and patients with apolipoprotein A-I (apoA-I) deficiency, apoE deficiency, or TD in terms of the plasma capacity to induce the efflux of [3H]-cholesterol from normal and TD fibroblasts and to esterify this cell-derived cholesterol. Compared with normal fibroblasts, TD fibroblasts released a significantly smaller fraction of [3H]-cholesterol into normal, high-density lipoprotein (HDL)-deficient, and apoE-deficient plasmas. Supplementation of apoE-deficient plasma with exogenous apoE normalized the cholesterol efflux from normal cells but did not fully restore the reduced cholesterol efflux from TD fibroblasts. Compared with control plasma, HDL- and apoE-deficient plasmas had a significantly reduced activity to esterify cell-derived cholesterol. Cholesterol derived from TD fibroblasts was less available for esterification in either patient or normal plasmas than cholesterol derived from normal cells. The esterification defect of TD cell-derived cholesterol was more pronounced in patient plasmas than in control plasma. We conclude that (1) apoA-I and, to a lesser degree, apoE are important determinants of the cholesterol efflux and esterification capacity of plasma, (2) TD fibroblasts have a reduced capacity to release cholesterol into the plasma, and (3) TD cell-derived cholesterol is less available for esterification in plasma than cholesterol from normal fibroblasts. The absence of distinct apoA-I- or apoE-containing subclasses aggravates the defective efflux and esterification of cholesterol derived from TD cells.
- Find related publications in this database (using NLM MeSH Indexing)
- Adult -
- Aged -
- Apolipoproteins E - blood
- Cells, Cultured - blood
- Cholesterol - blood
- Culture Media - blood
- Electrophoresis, Gel, Two-Dimensional - blood
- Esterification - blood
- Female - blood
- Fibroblasts - metabolism
- Humans - metabolism
- Lipids - blood
- Lipoproteins, HDL - blood
- Male - blood
- Middle Aged - blood
- Tangier Disease - blood