Nascent HDL formation by hepatocytes is reduced by the concerted action of serum amyloid A and endothelial lipase

Joanne M. Wroblewski, Anisa Jahangiri, Ailing Ji, Frederick C. De Beer, Deneys R. Van Der Westhuyzen, Nancy R. Webb

Research output: Contribution to journalArticlepeer-review

24 Scopus citations


Inflammation is associated with significant decreases in plasma HDL-cholesterol (HDL-C) and apoA-I levels. Endothelial lipase (EL) is known to be an important determinant of HDL-C in mice and in humans and is upregulated during inflammation. In this study, we investigated whether serum amyloid A (SAA), an HDL apolipoprotein highly induced during inflammation, alters the ability of EL to metabolize HDL. We determined that EL hydrolyzes SAAenriched HDL in vitro without liberating lipid-free apoA-I. Coexpression of SAA and EL in mice by adenoviral vector produced a significantly greater reduction in HDL-C and apoA-I than a corresponding level of expression of either SAA or EL alone. The loss of HDL occurred without any evidence of HDL remodeling to smaller particles that would be expected to have more rapid turnover. Studies with primary hepatocytes demonstrated that coexpression of SAA and EL markedly impeded ABCA1-mediated lipidation of apoA-I to form nascent HDL. Our findings suggest that a reduction in nascent HDL formation may be partly responsible for reduced HDL-C during inflammation when both EL and SAA are known to be upregulated.

Original languageEnglish
Pages (from-to)2255-2261
Number of pages7
JournalJournal of Lipid Research
Issue number12
StatePublished - Dec 2011


  • ATP-binding cassette transporter A1
  • Apolipoprotein A-I
  • Cholesterol
  • Inflammation

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Cell Biology


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