Cytokines decrease apolipoprotein accumulation in medium from Hep G2 cells. Arterioscler Thromb 1994 Jan;14(1):8-13
Date
01/01/1994Pubmed ID
8274481DOI
10.1161/01.atv.14.1.8Scopus ID
2-s2.0-0028047714 (requires institutional sign-in at Scopus site) 174 CitationsAbstract
Cytokines, important biochemical mediators of inflammation, cause a rapid fall in the plasma concentration of cholesterol in vivo. One mechanism by which cytokines may cause acquired hypocholesterolemia is by decreasing the hepatic synthesis and secretion of apolipoproteins. To test this hypothesis, we incubated Hep G2 cells with human recombinant tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6. Each of the cytokines resulted in a dose-related reduction in the concentrations of apolipoprotein (apo) A-I, apoB, and lecithin:cholesterol acyltransferase (LCAT) activity in the medium after 24 hours of incubation. The effect of cytokines on apolipoprotein accumulation was not affected by preincubation of Hep G2 cells with fatty acids. Cytokines decreased the concentration of cellular apoA-I mRNA in a dose-related fashion but did not affect cellular concentrations of apoB mRNA. The concentrations of triglyceride and cholesterol were also reduced in the medium of cells incubated with cytokines. Total cell sterol synthesis rates were calculated by [14C]acetate incorporation. Cells incubated with interleukin-6 had a 31% increase in sterol synthesis rate but a 41% decrease in sterol secretion. These data suggest that these cytokines can decrease the hepatic synthesis and/or secretion of apolipoproteins and that this may explain, in part, the acquired hypocholesterolemia seen during acute and chronic inflammation.
Author List
Ettinger WH, Varma VK, Sorci-Thomas M, Parks JS, Sigmon RC, Smith TK, Verdery RBAuthor
Mary Sorci Thomas PhD Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Apolipoprotein A-IApolipoproteins
Apolipoproteins B
Cell Line
Cholesterol
Culture Media
Cytokines
Docosahexaenoic Acids
Glucosephosphate Dehydrogenase
Humans
Interleukin-1
Interleukin-6
Linoleic Acid
Linoleic Acids
Palmitic Acid
Palmitic Acids
Phosphatidylcholine-Sterol O-Acyltransferase
RNA, Messenger
Triglycerides
Tumor Necrosis Factor-alpha









