FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2046847329> ?p ?o ?g. }

• W2046847329 endingPage "128" @default.
• W2046847329 startingPage "120" @default.
• W2046847329 abstract "Plasma inflammatory cytokines are elevated in obese subjects as well as in those with type 2 diabetes. This presumably results in systemic insulin resistance, characterized by a pro-atherogenic plasma lipid profile and reduced apolipoprotein AI (apoAI) protein levels. To determine how cytokine-mediated insulin resistance suppresses apoAI gene expression, we investigated the effect of tumor necrosis factor alpha (TNF alpha) and interleukin-1beta (IL-1beta) on apoAI protein, mRNA, and transcriptional activity in the human hepatoma cell line HepG2. ApoAI secretion was suppressed in a dose-dependent manner in HepG2 cells treated with both cytokines. ApoAI protein levels were 2892+/-22.0, 2263+/-117, 2458+/-25.0, 3401+/-152, 2333+/-248, 1520+/-41.5 and 956.0+/-11.0 arbitrary units (AU) in cells treated with 0, 0.3, 1.0, 3.0, 10, 30, and 100 ng/ml TNF alpha, achieving statistical significance in the 30 and 100 ng/ml range (P<0.0009). ApoAI protein levels were 4055+/-360, 3697+/-101, 3347+/-327, 1561+/-33.0, 1581+/-182, 810.0+/-59.5, and 1766+/-717 AU in cells treated with similar doses of IL-1beta, achieving statistical significance within the range of 3-100 ng/ml (P<0.02). ApoAI mRNA levels were suppressed 50.8% in HepG2 cells treated with 30 ng/ml TNF alpha for 24 h (P<0.05), and remained suppressed for up to 96 h. Similarly, treatment of cells with 30 ng/ml IL-1beta for 24 h, resulted in 42.9% reduction in apoAI mRNA levels (P<0.05) and remained suppressed for up to 96 h. In order to determine if the effect of TNF alpha and IL-1beta occurs at the transcriptional level, HepG2 cells were transfected with a chloramphenicol acetyltransferase (CAT) reporter gene plasmid containing the full-length apoAI promoter, and after 24 h, treated with TNF alpha (30 ng/ml), IL-1beta (30 ng/ml), or both cytokines. CAT activity was suppressed by both cytokines (24.0+/-1.9% acetylation in control cells vs. 5.6+/-1.2% (P<0.0004), 10.2+/-1.5% (P<0.0006), and 3.9+/-0.9% acetylation (P<0.0002) in cells treated with TNF alpha, IL-1beta, and the combination of both cytokines, respectively) suggesting that cytokine-mediated suppression occurs at the transcriptional level. Using a series of apoAI deletion constructs, the cytokine response element was mapped between nucleotides -325 and -186 (relative to the transcriptional start site). This region contains a previously identified and characterized cis-element, site A, which binds several different transcription factors. Finally, electrophoretic mobility shift assays (EMSA) showed that TNF alpha treatment of HepG2 cells is associated with reduced nuclear factor binding to site A. These studies suggest that inflammatory cytokines down-regulate apoAI expression at least partly through inhibition of binding of the nuclear factors to site A of the apoAI promoter." @default.
• W2046847329 created "2016-06-24" @default.
• W2046847329 creator A5037959449 @default.
• W2046847329 creator A5048385302 @default.
• W2046847329 creator A5075060708 @default.
• W2046847329 creator A5076724444 @default.
• W2046847329 creator A5080123196 @default.
• W2046847329 creator A5090355608 @default.
• W2046847329 date "2003-10-01" @default.
• W2046847329 modified "2023-10-11" @default.
• W2046847329 title "Suppression of apolipoprotein AI gene expression in HepG2 cells by TNF α and IL-1β" @default.
• W2046847329 cites W1523608977 @default.
• W2046847329 cites W1533904683 @default.
• W2046847329 cites W1549577793 @default.
• W2046847329 cites W1552471169 @default.
• W2046847329 cites W1764140709 @default.
• W2046847329 cites W180170051 @default.
• W2046847329 cites W1876911723 @default.
• W2046847329 cites W1898196512 @default.
• W2046847329 cites W1962343248 @default.
• W2046847329 cites W1969050011 @default.
• W2046847329 cites W1974033843 @default.
• W2046847329 cites W1975893519 @default.
• W2046847329 cites W1979669454 @default.
• W2046847329 cites W1987040411 @default.
• W2046847329 cites W1987522063 @default.
• W2046847329 cites W1995640339 @default.
• W2046847329 cites W1999129844 @default.
• W2046847329 cites W2005427150 @default.
• W2046847329 cites W2009818179 @default.
• W2046847329 cites W2010468331 @default.
• W2046847329 cites W2011836510 @default.
• W2046847329 cites W2014669590 @default.
• W2046847329 cites W2022961230 @default.
• W2046847329 cites W2023620533 @default.
• W2046847329 cites W2029284394 @default.
• W2046847329 cites W2033283522 @default.
• W2046847329 cites W2042087846 @default.
• W2046847329 cites W2045359842 @default.
• W2046847329 cites W2048272531 @default.
• W2046847329 cites W2051015298 @default.
• W2046847329 cites W2054851194 @default.
• W2046847329 cites W2068853602 @default.
• W2046847329 cites W2069968362 @default.
• W2046847329 cites W2070393128 @default.
• W2046847329 cites W2071781621 @default.
• W2046847329 cites W2088622701 @default.
• W2046847329 cites W2096252794 @default.
• W2046847329 cites W2100837269 @default.
• W2046847329 cites W2101108802 @default.
• W2046847329 cites W2113868760 @default.
• W2046847329 cites W2119983302 @default.
• W2046847329 cites W2129316761 @default.
• W2046847329 cites W2130078845 @default.
• W2046847329 cites W2135427256 @default.
• W2046847329 cites W2144206181 @default.
• W2046847329 cites W2144512169 @default.
• W2046847329 cites W2167634393 @default.
• W2046847329 cites W2179984620 @default.
• W2046847329 cites W2184409524 @default.
• W2046847329 cites W2411826498 @default.
• W2046847329 cites W4236102227 @default.
• W2046847329 cites W4245236743 @default.
• W2046847329 cites W4247801454 @default.
• W2046847329 cites W4249156097 @default.
• W2046847329 cites W4293247451 @default.
• W2046847329 cites W55452206 @default.
• W2046847329 doi "https://doi.org/10.1016/j.bbagen.2003.08.004" @default.
• W2046847329 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/14572909" @default.
• W2046847329 hasPublicationYear "2003" @default.
• W2046847329 type Work @default.
• W2046847329 sameAs 2046847329 @default.
• W2046847329 citedByCount "59" @default.
• W2046847329 countsByYear W20468473292012 @default.
• W2046847329 countsByYear W20468473292013 @default.
• W2046847329 countsByYear W20468473292015 @default.
• W2046847329 countsByYear W20468473292016 @default.
• W2046847329 countsByYear W20468473292017 @default.
• W2046847329 countsByYear W20468473292018 @default.
• W2046847329 countsByYear W20468473292019 @default.
• W2046847329 countsByYear W20468473292020 @default.
• W2046847329 countsByYear W20468473292022 @default.
• W2046847329 countsByYear W20468473292023 @default.
• W2046847329 crossrefType "journal-article" @default.
• W2046847329 hasAuthorship W2046847329A5037959449 @default.
• W2046847329 hasAuthorship W2046847329A5048385302 @default.
• W2046847329 hasAuthorship W2046847329A5075060708 @default.
• W2046847329 hasAuthorship W2046847329A5076724444 @default.
• W2046847329 hasAuthorship W2046847329A5080123196 @default.
• W2046847329 hasAuthorship W2046847329A5090355608 @default.
• W2046847329 hasConcept C104317684 @default.
• W2046847329 hasConcept C105580179 @default.
• W2046847329 hasConcept C11988809 @default.
• W2046847329 hasConcept C126322002 @default.
• W2046847329 hasConcept C134018914 @default.
• W2046847329 hasConcept C150194340 @default.
• W2046847329 hasConcept C159110408 @default.
• W2046847329 hasConcept C17991360 @default.

• next