Expression of human hepatic lipase negatively impacts apolipoprotein A-I production in primary hepatocytes from Lipc-null mice

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DOIResolve DOI: http://doi.org/10.7555/JBR.28.20130184
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TypeArticle
Journal titleJournal of Biomedical Research
ISSN1674-8301
Volume28
Issue3
Pages201212; # of pages: 12
Subjectapolipoprotein A1; apolipoprotein E; liver triacylglycerol lipase; Adenoviridae; animal cell; cell fractionation; cell surface; cellular distribution; controlled study; endoplasmic reticulum; female; gene transfer; genetic transfection; HepG2 cell line; human cell; immunoblotting; liver cell; microsome; mouse; null cell; protein expression; protein secretion; secretory pathway
AbstractThis study aimed to examine whether expression of human hepatic lipase (hHL) exerted an intracellular effect on hepatic production of apolipoprotein (apo) A-I. The levels of secreted and cell-associated apoA-I were contrasted between primary hepatocytes isolated from Lipc-null and C57BL/6 mice, and between Lipc-null hepatocytes transfected with either hHL-encoding or control adenovirus. An HSPG-binding deficient hHL protein (hHLmt) was used to determine the impact of cell surface binding on HL action. Accumulation of apoA-I in conditioned media of primary hepatocytes isolated from Lipc-null mice was increased as compared to that from C57BL/6 mice. Metabolic labeling experiments showed that secretion of 35S-apoA-I from Lipc-null cells was significantly higher than that from C57BL/6 cells. Expression of hHL in Lipc-null hepatocytes, through adenovirus-mediated gene transfer, resulted in decreased synthesis and secretion of 35S-apoA-I, but not 35S-apoE, as compared with cells transfected with control adenovirus. Expression of HSPG-binding deficient hHLmt in Lipc-null cells also exerted an inhibitory effect on apoA-I production, even though hHLmt displayed impaired exit from the endoplasmic reticulum as compared with hHL. Subcellular fractionation revealed that expression of hHL or hHLmt led to increased microsome-association of apoA-I relative to non-transfected control. Expression of hHL negatively impacts hepatic production of apoA-I.
Publication date
PublisherNational Center for Biotechnology Information
LanguageEnglish
AffiliationNational Research Council Canada (NRC-CNRC); Human Health Therapeutics
Peer reviewedYes
NPARC number21275578
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Record identifier5fefec5e-02ab-497e-b210-5711e1e32667
Record created2015-07-14
Record modified2016-05-09
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