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题目:: Transcription profiling of classically activated, alternatively activated, and naive mouse macrophages
ID:
状态:: 发布时间Sept. 15, 2006 , 更新时间 June 10, 2011
物种:: Mus musculus
摘要:: Complex interplay between T helper (Th) cells and macrophages contributes to the formation and progression of atherosclerotic plaques. While Th1 cytokines promote inflammatory activation of lesion macrophages, Th2 cytokines attenuate macrophage-mediated inflammation and enhance their repair functions. In spite of its biologic importance, the biochemical and molecular basis of how Th2 cytokines promote maturation of anti-inflammatory macrophages is not understood. We show here that in response to interleukin-4 (IL-4), signal transducer and activator of transcription 6 (STAT6) and PPARg-coactivator-1b (PGC-1b) induce macrophage programs for fatty acid oxidation and mitochondrial biogenesis. Transgenic expression of PGC-1b primes macrophages for alternative activation and strongly inhibits proinflammatory cytokine production, whereas inhibition of oxidative metabolism or RNAi-mediated knockdown of PGC-1b attenuates this immune response. These data elucidate a molecular pathway that directly links mitochondrial oxidative metabolism to the anti-inflammatory program of macrophage activation, suggesting a potential role for metabolic therapies in treating atherogenic inflammation. Total RNA was prepared from three independent experimental replicates using Trizol reagent (Invitrogen) and validated by northern blot. Microarray experiments were performed with 20-25 ?g of total RNA, which was labelled with fluorescent nucleotides and hybridized to murine cDNA slides. Hybridized slides were interrogated via an Agilent scanner. Cells were activated with either interleukin-4, interferon-gamma/lipo-polysaccharide, or vehicle in low-glucose media.
实验种类:: transcription profiling by array
样本量:: 0
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数据号:: E-SMDB-3728
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