Clinical Chemistry Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Clinical Chemistry 45: 1567-1569, 1999;
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit an electronic Letter to
the Editor about this paper
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (12)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Escolà-Gil, J. C.
Right arrow Articles by Blanco-Vaca, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Escolà-Gil, J. C.
Right arrow Articles by Blanco-Vaca, F.
Related Collections
Right arrow Lipids, Lipoproteins, and Cardiovascular Risk Factors
(Clinical Chemistry. 1999;45:1567-1569.)
© 1999 American Association for Clinical Chemistry, Inc.

Technical Briefs

Pitfalls of Direct HDL-Cholesterol Measurements in Mouse Models of Hyperlipidemia and Atherosclerosis

Joan Carles Escolà-Gil1,2, Oscar Jorba1, Josep Julve-Gil1,2, Francesc González-Sastre1,3, Jordi Ordóñez-Llanos1,3 and Francisco Blanco-Vaca1,2,a

1 Servei de Bioquímica and
2 Institut de Recerca de l'Hospital de la Santa Creu i Sant Pau, C/Antoni M. Claret 167, 08025 Barcelona, Spain;
3 Departament de Bioquímica i Biologia Molecular, Universitat Autònoma de Barcelona, 0825 Barcelona, Spain;
a author for correspondence: fax 34-93-2919196,

Mice have become important models in lipoprotein and atherosclerosis research (1)(2). Certain strains of mice, such as C57BL/6, develop hyperlipidemia—as a result of the accumulation in plasma of cholesterol-rich remnant particles—and aortic atherosclerosis when fed a high fat, high cholesterol diet (atherogenic diet) (1)(2). Apolipoprotein E-deficient [apoE(-)] mice also develop hyperlipidemia—as a result of the accumulation of remnant lipoproteins that float mainly as VLDL and intermediate-density lipoprotein—and massive atherosclerosis even when they are fed a diet of regular chow, which is only 4% fat (1). These two mouse models currently are being used to study the effect of gene expression in atherosclerosis with at least two main goals: to understand the mechanisms underlying the genesis and progression of atherosclerosis, and to investigate the feasibility of different genetic and pharmacological interventions to stop or regress atherosclerosis and prevent its complications.

Previous studies have already been instrumental in defining the role of the different HDL particles with respect to atherosclerosis (3)(4). Indeed, any study of this kind requires accurate and reproducible measurement of the cholesterol concentrations associated with the different lipoprotein fractions. For these purposes, fast protein liquid chromatography (FPLC) has been used to isolate HDL and to measure its cholesterol content (HDL-C) (5). This procedure can be performed using smaller volumes of plasma than with ultracentrifugation, which usually requires the use of plasma pooled from different mice. However, both preparative methods are labor-intensive. Because current experiments in mice require an increasingly larger number of animals, HDL has been also isolated by precipitation of apolipoprotein B (apoB)-containing lipoproteins using a variety of reagents (3). Recently, several new direct methods for testing HDL-C have been developed and adapted to many clinical chemistry laboratories (6. . . [Full Text of this Article]


Acknowledgments


References




The following articles in journals at HighWire Press have cited this article:


Home page
 J BiochemHome page
S. Acin, M. A. Navarro, J. M. Arbones-Mainar, N. Guillen, A. J. Sarria, R. Carnicer, J. C. Surra, I. Orman, J. C. Segovia, R. d. l. Torre, et al.
Hydroxytyrosol Administration Enhances Atherosclerotic Lesion Development in Apo E Deficient Mice
J. Biochem., September 1, 2006; 140(3): 383 - 391.
[Abstract] [Full Text] [PDF]

Home page
 Clin. Chem.Home page
G. R. Warnick, M. Nauck, and N. Rifai
Evolution of Methods for Measurement of HDL-Cholesterol: From Ultracentrifugation to Homogeneous Assays
Clin. Chem., September 1, 2001; 47(9): 1579 - 1596.
[Abstract] [Full Text] [PDF]

Home page
 J. Lipid Res.Home page
J. C. Escolà-Gil, J. Julve, A. Marzal-Casacuberta, J. Ordóñez-Llanos, F. González-Sastre, and F. Blanco-Vaca
ApoA-II expression in CETP transgenic mice increases VLDL production and impairs VLDL clearance
J. Lipid Res., February 1, 2001; 42(2): 241 - 248.
[Abstract] [Full Text]

Home page
 Clin. Chem.Home page
J. Ordonez-Llanos, A. M. Wagner, R. Bonet-Marques, J. L. Sanchez-Quesada, F. Blanco-Vaca, and F. Gonzalez-Sastre
Which Cholesterol Are We Measuring with the Roche Direct, Homogeneous LDL-C Plus Assay?
Clin. Chem., January 1, 2001; 47(1): 124 - 126.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1999 by the American Association for Clinical Chemistry.