摘要: Purpose: Chronic inflammation is a central feature of many human diseases, including atherosclerosis. The transcriptional co-regulator RIP140 (Receptor-interacting protein of 140 kDa) is a co-repressor for nuclear receptors and regulates lipid and glucose metabolism in adipocytes and skeletal muscle. RIP140 may also act as a co-activator for NFkB, driving pro-inflammatory responses in murine macrophages. The aim of this study is to elucidate the regulation and the role of RIP140 in the inflammatory response triggered by tumour necrosis factor a (TNFa) in endothelial cells (EC). Methods and results: Our data demonstrate that RIP140 is up-regulated at the transcriptional and translational level by TNFa in human umbilical vein EC (HUVEC)(p, 0.01). In silico analysis revealed two NFkB binding sites within the RIP140 promoter. NFkB inhibition with BAY11-7085, or by overexpression of the IkBa super-repressor …
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