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. Author manuscript; available in PMC: 2008 Nov 25.
Published in final edited form as: Nature. 2007 May 21;447(7148):1116–1120. doi: 10.1038/nature05894

Figure 1.

Figure 1

PPARγ regulates alternative macrophage activation. a, Decreased induction of arginase activity by IL-4 in PPARγ null macrophages. BMDM from control and Mac-PPARγ KO mice were stimulated with IL-4 (10ng/ml) for 24 or 48 hours prior to quantification of cell-associated arginase activity. b, Activation of arginase I promoter by PPARγ/RXR heterodimers. c, PPARγ is required for suppression of IL-6 production in alternatively activated macrophages. Macrophages pre-treated with IL-4 (10 ng/ml) for 24 hours were subsequently stimulated with LPS (5 ng/ml) for 6 hours (TNFα) or 24 hours (IL-6). d, PPARγ is required for macrophage oxidative metabolism. Fatty acid oxidation rates were quantified in control, PPARδ null and PPARγ null BMDMs 96 hours after stimulation with IL-4. e-f, IL-4 fails to induce mitochondrial biogenesis in PPARγ deficient macrophages, as measured by (e) Mito Tracker Green and (f) CytC and VDAC1 protein levels. Equivalent loading was confirmed by immunoblotting for β-actin. Rosiglitazone (Rosi).