PubMed:10208867 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/10208867","sourcedb":"PubMed","sourceid":"10208867","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/10208867","text":"Angiotensin II activates the proinflammatory transcription factor nuclear factor-kappaB in human monocytes.\nThe renin-angiotensin system may contribute to the pathogenesis of atherosclerosis. A common feature of all stages of atherosclerosis is inflammation of the vessel wall. The transcription factor nuclear factor-kappaB (NF-kappaB) participates in most signaling pathways involved in inflammation. This study therefore examined the effect of angiotensin (ANG) II on NF-kappaB activation in monocytic cells, a major cellular component of human atheroma, by electrophoretic mobility shift assay. ANG II, like TNFalpha, caused rapid activation of NF-kappaB in human mononuclear cells isolated from peripheral blood by Ficoll density gradient. This ANG II effect was blocked by the angiotensin AT1 receptor antagonist losartan. Specificity of ANG II-induced NF-kappaB activation was ascertained by supershift and competition experiments. Moreover, ANG II stimulated NF-kappaB activation in human monocytes, but not in lymphocytes from the same preparation. 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