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• W1620587130 startingPage "963" @default.
• W1620587130 abstract "The pathogenesis of septicemia can be triggered by LPS, a potent stimulus for PG synthesis. The enzyme cyclooxygenase (COX) is a rate-limiting step in PG production. COX exists as two isoforms: COX-1, which is constitutively expressed in most cell types, and COX-2, which is inducible by LPS and cytokines in a variety of cells. In this study we determined the role of the proinflammatory cytokines IL-1 beta and TNF-alpha released by LPS-stimulated U937 human macrophages in the regulation of COX-2. Macrophages exposed to LPS showed a rapid and sustained expression of COX-2 mRNA and protein for up to 48 h, whereas PGE2 production was notably enhanced only after 12 h. LPS increased COX-2 gene transcription and activation of the transcription factor NF-kappa B in a transient manner. LPS-treated macrophages produced high levels of TNF-alpha and moderate amounts of IL-1 beta protein. However, neutralizing Abs against these cytokines had no effect on COX-2 mRNA and protein expression, nor did they affect the stability of COX-2 mRNA. Interestingly, in the presence of LPS or exogenous IL-1 beta, COX-2 transcripts were stabilized, and actinomycin D inhibited their degradation. Only when LPS or IL-1 beta was removed did COX-2 mRNA decay with a t1/2 of >/=5 h. In contrast, dexamethasone promoted a faster decay of the LPS-induced COX-2 transcripts (t1/2 = 2.5 h). These results clearly demonstrate that LPS can regulate COX-2 at both transcriptional and posttranscriptional levels independently from endogenous IL-1 beta and TNF-alpha in human macrophages." @default.
• W1620587130 created "2016-06-24" @default.
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• W1620587130 creator A5065044412 @default.
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• W1620587130 date "1999-07-15" @default.
• W1620587130 modified "2023-09-23" @default.
• W1620587130 title "Lipopolysaccharide modulates cyclooxygenase-2 transcriptionally and posttranscriptionally in human macrophages independently from endogenous IL-1 beta and TNF-alpha." @default.
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• W1620587130 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10395693" @default.
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