The generality and spectrum of chromatin-remodeling requirements for nuclear receptor function are unknown. We have characterized glucocorticoid receptor (GR) binding events and chromatin structural transitions across GR-induced or -repressed genes. This analysis reveals that GR binding invariably occurs at nuclease-accessible sites (DHS). A remarkable diversity of mechanisms, however, render these sites available for GR binding. Accessibility of the GR binding sites is either constitutive or hormone inducible. Within each category, some DHS sites require the Brg1-containing Swi/Snf complex, but others are Brg1 independent, implicating a different remodeling complex. The H2A.Z histone variant is highly enriched at both inducible and constitutive DHS sites and is subject to exchange during hormone activation. The DHS profile is highly cell specific, implicating cell-selective organization of the chromatin landscape as a critical determinant of tissue-selective receptor function. Furthermore, the widespread requirement for chromatin remodeling supports the recent hypothesis that the rapid exchange of receptor proteins occurs during nucleosome reorganization.

Interaction of the Glucocorticoid Receptor with the Chromatin Landscape

Endothelial primary cilia in areas of disturbed flow are at the base of atherosclerosis

Purpose of review Epigenetic regulation plays an essential role in cell differentiation, by allowing the establishment and maintenance of the gene-expression pattern of the mature cell type. Because of its importance in chronic diseases, adipogenesis is one of the best-studied differentiation processes. The hormonal and transcriptional cascades governing the differentiation of the adipocytes are well known, but the role of epigenetic mechanisms is only starting to emerge. In this review, we intend to summarize the recently described epigenetic events that participate in adipogenesis and their connections with the main factors that constitute the classical transcriptional cascade. Recent findings The advent of high-throughput technologies has made possible the exhaustive analysis of the epigenetic phenomenons taking place during adipogenesis. The cooperative recruitment of CCAAT/enhancer-binding protein (C/EBPβ) and other early proadipogenic transcription factors to transcription factor hotspots shortly after induction of adipogenesis is required to establish a transient epigenomic state that then informs the recruitment of the later adipogenic transcription factors peroxisome proliferator-activated receptor (PPARγ) and C/EBPα to their target genes. Summary Epigenetic marks and chromatin-modifying proteins contribute to adipogenesis and, through regulation of the phenotypic maintenance of the mature adipocytes, to the control of metabolism.

Epigenetic regulation of adipogenesis.

Our purpose was to determine if high-fat diet and treatment with a polyphenol regulate the acetylation of lysine-382 of p53, the site regulated by sirtuin-1, and apoptosis in the endothelium of the atherosclerotic lesion-prone mouse aortic arch. In cultured endothelial cells, 2 atherogenic stimuli, hydrogen peroxide and tumor necrosis factor-α, increased the acetylation of p53 lysine-382, and caspase-3 cleavage, an indicator of apoptotic signaling. The polyphenol, S17834, significantly prevented these changes. In low-density lipoprotein receptor-deficient mice, a high-fat diet increased, and treatment with S17834 attenuated early atherosclerotic lesions on the lesser curvature of the aortic arch. In wild-type C57BL6 mice fed the same diet, no atherosclerotic lesions were observed in this lesion-prone area, but p53 acetylation and caspase-3 cleavage increased in the endothelium. In high-fat fed mice, S17834 increased sirtuin-1 protein in the lesion-prone endothelium and prevented both the increase in p53 acetylation and caspase-3 cleavage without affecting blood lipids. These results indicate that high-fat diet increases and S17834 decreases the acetylation of p53 in lesion-prone aortic endothelial cells of normal mice independently of blood lipids, suggesting that the polyphenol may regulate endothelial cell p53 acetylation and apoptosis via local actions.

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High-fat diet increases and the polyphenol, S17834, decreases acetylation of the sirtuin-1-dependent lysine-382 on p53 and apoptotic signaling in atherosclerotic lesion-prone aortic endothelium of normal mice.

Placental PPARγ regulates spatiotemporally diverse genes and a unique metabolic network.

Regional determinants of arterial endothelial phenotype dominate the impact of gender or short-term exposure to a high-fat diet

Cell-Specific Determinants of PPARγ γγ γ Function in Adipocytes and Macrophages

two-channel high-density microarray experiments Comparison of different labeling methods for

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Regional determinants of arterial endothelial phenotype dominate the impact of gender or short-term exposure to a high-fat diet

Cell-Specific Determinants of PPARγ γγ γ Function in Adipocytes and Macrophages

two-channel high-density microarray experiments Comparison of different labeling methods for