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A more recent version of this article appeared on April 1, 2005

Papers In Press, published online ahead of print January 16, 2005
J. Lipid Res., doi:10.1194/jlr.M400165-JLR200
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Submitted on April 29, 2004
Revised on January 11, 2005
Accepted on January 14, 2005

Physiological importance of SR-BI in the in vivo metabolism of human HDL and LDL in male and female mice

Mathieu R. Brodeur, Vilayphone Luangrath, Geneviève Bourret, Louise Falstrault, and Louise Brissette

Sciences Biologiques, Université du Québec à Montréal, Montréal, Québec H3C 3P8

Corresponding Author: brodeur.mathieu{at}courrier.uqam.ca

The physiological role of murine scavenger receptor class B type I (SR-BI) was evaluated by in vivo clearances of human high and low density lipoproteins (HDL3 and LDL) in normal (+/+), heterozygous (+/-) and homozygous (-/-) SR-BI knockout (KO) male and female mice. Cholesteryl esters (CE) were removed faster than proteins, indicating a selective uptake process from both HDL3 and LDL in the three genotypes. Heterozygous and homozygous deficient male mice showed 40 and 80% losses of HDL-CE selective uptake, respectively. Similar data were obtained in female mice. In males, the loss of SR-BI resulted in the complete loss of LDL-CE selective uptake in the first phase of clearance, indicating again a strong implication of SR-BI. However, the second phase was characterized by an acceleration of CE disappearance in (-/-) SR-BI KO male mice. This phenomenon was even greater in females. Thus, SR-BI is the only murine receptor mediating HDL-CE selective uptake, while a SR-BI-independent pathway specific to LDL can rescue SR-BI deficiency. The analysis of LDL recovered 3 hours after injection in mice from different genotypes and genders revealed that LDL are significantly depleted in CE (reduction from 19 to 50% of the CE/protein ratios). A smaller LDL size in comparison with that of non-injected LDL was also detectable but was more evident for LDL recovered from normal male and female mice. All LDL preparations migrate faster than non-injected LDL on agarose-barbital gels. Thus both SR-BI dependent and independent pathways lead to substantial changes in LDL.


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