ApoB-containing lipoproteins in apoE-deficient mice are not metabolized by the class B scavenger receptor BI

Nancy R. Webb, Maria C. De Beer, Frederick C. De Beer, Deneys R. Van Der Westhuyzen

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


The scavenger receptor class B type I (SR-BI) recognizes a broad variety of lipoprotein ligands, including HDL, LDL, and oxidized LDL. In this study, we investigated whether SR-BI plays a role in the metabolism of cholesterol-rich lipoprotein remnants that accumulate in apolipoprotein E (apoE)-/- mice. These particles have an unusual apolipoprotein composition compared with conventional VLDL and LDL, containing mostly apoB-48 as well as substantial amounts of apoA-I and apoA-IV. To study SR-BI activity in vivo, the receptor was overexpressed in apoE-/- mice by adenoviral vector-mediated gene transfer. An ∼10-fold increase in liver SR-BI expression resulted in no detectable alterations in VLDL-sized particles and a modest depletion of cholesterol in intermediate density lipoprotein/LDL-sized lipoprotein particles. This decrease was not attributable to altered secretion of apoB-containon lipoproteins in SR-BI-overexpressing mice. To directly assess whether SR-BI metabolizes apoE-/- mouse lipoprotein remnants, in vitro assays were performed in both CHO cells and primary hepatocytes expressing high levels of SR-BI. This analysis showed a remarkable deficiency of these particles to serve as substrates for selective lipid uptake, despite high-affinity, high-capacity binding to SR-BI. Taken together, these data establish that SR-BI does not play a direct role in the metabolism of apoE-/- mouse lipoprotein remnants.

Original languageEnglish
Pages (from-to)272-280
Number of pages9
JournalJournal of Lipid Research
Issue number2
StatePublished - Feb 2004


  • Adenoviral vector
  • Apolipoprotein B
  • Apolipoprotein E
  • Hepatocytes
  • Lipoprotein
  • Lipoprotein metabolism
  • Selective lipid uptake

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Cell Biology


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