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Clinical Chemistry, Vol 40, 395-399, Copyright © 1994 by American Association for Clinical Chemistry
AJ Van den Broek, L Hollaar, HI Schaefer, A Van der Laarse, H Schuster, JC Defesche, JJ Kastelein and FM Van 't Hooft
Department of Cardiology, University Hospital, Leiden, The Netherlands.
Frostegard et al. (J Lipid Res 1990;31:37-44) demonstrated that the proliferation of the human monocyte cell line U937 is critically dependent on the uptake of low-density lipoprotein (LDL) via the apo B, E (LDL) receptor, a characteristic that was used to detect patients with familial defective apolipoprotein B-100 (FDB). Here we applied this principle to develop a simple and reproducible assay for the detection of patients with functionally defective LDL. We added serum to U937 cells in cholesterol-free incubation medium and determined the increase in cell number after a 72-h incubation at 37 degrees C by using an electronic cell counter. Sera from 10 normolipidemic individuals and from 34 patients with type IIa hyperlipoproteinemia stimulated the growth of U937 cells in proportion to the exogenous cholesterol concentration (r = 0.83, P < 0.001) and the LDL-cholesterol concentration (r = 0.81, P < 0.001). However, sera from 16 patients with FDB stimulated less cell proliferation than did sera from patients with type IIa hyperlipoproteinemia with equal LDL-cholesterol concentrations. With a 15% reduction in growth as the cutoff value, this test had a sensitivity and specificity for diagnosis of FDB of 87.5% and 100%, respectively. The improved U937 monocyte proliferation assay can be used for screening hypercholesterolemic patients to detect individuals with functionally defective LDL.
The following articles in journals at HighWire Press have cited this article:
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  G. Baillie, M. D. Owens, and G. W. Halbert A synthetic low density lipoprotein particle capable of supporting U937 proliferation in vitro J. Lipid Res., January 1, 2002; 43(1): 69 - 73. [Abstract] [Full Text] [PDF]
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B. Raungaard, F. Heath, P. S. Hansen, J. U. Brorholt-Petersen, H. K. Jensen, and O. Fargeman Flow Cytometric Assessment of LDL Ligand Function for Detection of Heterozygous Familial Defective Apolipoprotein B-100 Clin. Chem., February 1, 2000; 46(2): 224 - 233. [Abstract] [Full Text] [PDF]
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 H. H.-J. Schmidt, M. Stuhrmann, R. Shamburek, C. K. Schewe, M. Ebhardt, L. A. Zech, C. Büttner, M. Wendt, U. Beisiegel, H. B. Brewer, et al. Delayed Low Density Lipoprotein (LDL) Catabolism Despite a Functional Intact LDL-Apolipoprotein B Particle and LDL-Receptor in a Subject with Clinical Homozygous Familial Hypercholesterolemia J. Clin. Endocrinol. Metab., June 1, 1998; 83(6): 2167 - 2174. [Abstract] [Full Text]
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M.-L. Choong, E. S. C. Koay, K.-L. Khoo, M.-C. Khaw, and S. K. Sethi Denaturing gradient-gel electrophoresis screening of familial defective apolipoprotein B-100 in a mixed Asian cohort: two cases of arginine3500 -> tryptophan mutation associated with a unique haplotype Clin. Chem., June 1, 1997; 43(6): 916 - 923. [Abstract] [Full Text] [PDF]
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 J. R. Schaefer, H. Scharnagl, M. W. Baumstark, H. Schweer, L. A. Zech, H. Seyberth, K. Winkler, A. Steinmetz, and W. Marz Homozygous Familial Defective Apolipoprotein B-100: Enhanced Removal of Apolipoprotein E–Containing VLDLs and Decreased Production of LDLs Arterioscler Thromb Vasc Biol, February 1, 1997; 17(2): 348 - 353. [Abstract] [Full Text]
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