ArticleAnnals of the rheumatic diseases2006
Differential influence of p38 mitogen activated protein kinase (MAPK) inhibition on acute phase protein synthesis in human hepatoma cell lines.
Article in Annals of the rheumatic diseases, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Fibrinogen and tumors.Frontiers in oncology · 2024Review
- Markers of angiogenesis and macrophage products for predicting disease course and monitoring vascular inflammation in giant cell arteritis.Rheumatology (Oxford, England) · 2019Article
- Systems Analysis of the Complement-Induced Priming Phase of Liver Regeneration.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Hepatitis C virus core protein interacts with fibrinogen-beta and attenuates cytokine stimulated acute-phase response.Hepatology (Baltimore, Md.) · 2010Article
- Effect of wine phenolics on cytokine-induced C-reactive protein expression.Journal of thrombosis and haemostasis : JTH · 2007Article
- Bioinformatics analysis of the early inflammatory response in a rat thermal injury model.BMC bioinformatics · 2007Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInhibition of intracellular signal transduction is considered to be an interesting target for treatment in inflammation. p38 MAPK inhibitors, especially, have been developed and are now in phase II clinical trials for rheumatoid arthritis (RA).
objectiveTo investigate the influence of p38 MAPK inhibition on acute phase protein (APP) production, which is dependent on both JAK/STAT and p38 MAPK pathways.
methodsThe effects of p38 MAPK inhibition on APP production and mRNA expression in four human hepatoma cell lines was investigated, after stimulation with interleukin (IL)6 and/or IL1beta or tumour necrosis factor alpha.
resultsTwo out of four cell lines produced C reactive protein (CRP), especially after combined IL6 and IL1beta stimulation. CRP production was significantly inhibited by the p38 MAPK specific inhibitor RWJ 67657 at 1 micromol/l, which is pharmacologically relevant. Fibrinogen production was also inhibited at 1 micromol/l in all cell lines. Serum amyloid A (SAA) was produced in all four lines. In contrast with CRP, SAA production was not inhibited by RWJ 67657 at 1 micromol/l.
conclusionProduction and mRNA expression of CRP and fibrinogen, but not SAA production and mRNA expression, were significantly inhibited by p38 MAPK specific inhibitor in hepatoma cell lines. For p38 MAPK inhibitor treatment in RA SAA might be a better marker of disease activity than CRP and fibrinogen, because SAA is not directly affected by p38 MAPK inhibition.
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