NDLI: Cytokine regulation of low density lipoprotein receptor gene transcription in HepG2 cells.

Content Provider	Journal of Biological Chemistry (JBC)
Author	Stopeck, A. T. Nicholson, A. C. Mancini, F. P. Hajjar, D. P.
Abstract	Elevated plasma levels of cytokines have been demonstrated in inflammatory, malignant, and infectious diseases. These disease states are often associated with abnormal lipid metabolism and reductions in plasma cholesterol levels. To determine if inflammatory cytokines could influence hepatic lipid metabolism, we evaluated low density lipoprotein (LDL) receptor function and gene expression in cytokine stimulated HepG2 cells, a hepatoblastoma-derived cell line which shares many functional similarities with normal hepatocytes. Tumor necrosis factor-alpha (TNF) and interleukin-1 beta (IL-1) increased LDL binding to HepG2 cells in a dose-responsive manner. Other cytokines including macrophage-colony stimulating factor, granulocyte macrophage-colony stimulating factor, and gamma-interferon had no significant effects on LDL binding. Increased binding in response to TNF or IL-1 was paralleled by increased steady-state levels of LDL receptor mRNA. Evaluation of LDL receptor mRNA half-life revealed no significant change in mRNA stability between control and TNF- or IL-1-stimulated cells. A fusion gene construct consisting of 1563 base pairs of the 5'-flanking DNA of the human LDL receptor gene was coupled to a luciferase reporter gene, transfected into HepG2 cells, and promoter activity was assayed after TNF and IL-1 challenge to the cells. TNF and IL-1 increased promoter activity 200-400%, while treatment with LDL inhibited promoter activity by 70-85%. TNF or IL-1 co-incubation with LDL could not override transcriptional inhibition by LDL. Pretreatment with cycloheximide prevented induction of LDL receptor mRNA by TNF, but not by IL-1, suggesting stimulation of LDL receptor transcription by TNF requires protein synthesis. We propose that TNF and IL-1, acting via distinct signal transduction pathways, increase surface LDL receptors by increasing gene transcription. Our findings suggest that cytokine-induced hypocholesterolemia may be related to TNF and/or IL-1 stimulation of hepatic LDL receptor gene expression and function.
Related Links	http://www.jbc.org/content/268/23/17489.abstract
Ending Page	17494
Starting Page	17489
Page Count	6
File Format	HTM / HTML PDF
ISSN	00219258
Journal	Journal of Biological Chemistry (JBC)
Issue Number	23
Volume Number	268
e-ISSN	1083351X
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	1993-08-15
Access Restriction	Open
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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