Journal of nutrigenetics and nutrigenomics 20130206 1
BACKGROUND/AIMS: Saturated fatty acids (SFA) are widely thought to induce inflammation in adipose tissue (AT), while monounsaturated fatty acids (MUFA) are purported to have the opposite effect; however, it is unclear if individual SFA and MUFA behave similarly. Our goal was to examine adipocyte transcriptional networks regulated by individual SFA (palmitic acid, PA; stearic acid, SA) and MUFA (palmitoleic acid, PMA; oleic acid, OA). METHODS: Differentiated preadipocytes were treated with either ...[more]
Project description:This SuperSeries is composed of the following subset Series:; GSE8679: Gene expression in mouse white adipose tissue; GSE8681: Gene expression in mouse 3T3-L1 adipocyte tissue culture treated with CLA; GSE8682: Gene expression in mouse 3T3-L1 adipocyte tissue culture treated with tunicamycin; GSE8683: Gene expression in 3T3-L1 mouse tissue (preadipocytes) treated with Trans-10,Cis-12 conjugated linoleic acid(t10c12 CLA); GSE8684: Gene expression in mouse 3T3-L1 adipocyte tissue culture treated with cis-9,trans-11 conjugated linoleic acid(c9t11 CLA) Experiment Overall Design: Refer to individual Series
Project description:This study was undertaken to assess the similarities (or differences) between the well-established PPARγ agonist Rosiglitazone and Non-steroidal anti-inflammatory drugs (NSAIDs) diclofenac, indomethacin and ibuprofen, as well as the partial agonist GQ16 at the transcriptome level. Assessment of NSAID and GQ16 activities in PPARγ-dependent 3T3-L1 cells reveals that NSAIDs and GQ16 display similar effects toward PPARγ-dependent target genes in a manner similar to that of Rosiglitazone. Overall design: Murine 3T3-L1 preadipocytes were differentiated into adipocytes (7 days), then treated with DMSO (control), 100nM rosiglitazone, 25μM sodium diclofenac, 10μM indomethacin, 75μM ibuprofen, or 10μM GQ16 for 24 hours, after which total RNA was isolated.
Project description:DNA methylation plays a crucial role in the regulation of gene transcription. In this study, using MeDIP-seq experiment, we report the mapping of DNA methylation in undifferentiated 3T3-L1 cells (preadipocytes). Examination of DNA methylation pattern in undifferentiated 3T3-L1 cells (preadipocytes)
Project description:In this setup we have used RNA-seq to define which cAMP-induced genes are dependent on activity of the JAK kinases or MDM2. Also, we mapped binding of the coactivator CRTC2 to DNA upon forskolin stimulation. Overall design: Global gene expression analysis in 3T3-L1 preadipocytes as well as p53-/- and p53-/-;mdm2-/- MEFs treated with JAK inhibitor and/or forskolin. Furthermore, we have performed ChIP on CRTC2 in 3T3-L1 preadipocytes stimulated with forskolin and pretreated with either vehicle or the JAK inhibitor P6.
Project description:Obesity is often associated with a low-grade systemic inflammation state that contributes to the development of insulin resistance and atherosclerotic complications. This is usually coupled with increased macrophage infiltration in the adipose tissue and a defect in adipocyte differentiation that results in accumulation of hypertrophic fat cells characterized by a deregulated pattern of adipokine expression. Here we show that knockdown of histone demethylase lsd1 in 3T3-L1 preadipocytes results in defective adipogenesis and derepression of an inflammatory program in these cells. The dataset consists of four sample groups:  3T3-L1 preadipocytes (passage 19) transfected with a control scrambled siRNA at 24h after transfection (siC.24h),  3T3-L1 preadipocytes (p.19) transfected with a siRNA directed against LSD1 at 24h after transfection (siLsd1.24h),  3T3-L1 preadipocytes (p.21) transfected with a control scrambled siRNA at 48h after transfection (siC.48h), and  3T3-L1 preadipocytes (p.21) transfected with a siRNA directed against LSD1 at 48h after transfection (siLsd1.48h). The 24h sample groups (siC.24h and siLsd1.24h) consist of two biological replicate samples; the 48h sample groups (siC.48h and siLsd1.48h) consist of three biological replicate samples. Each sample was hybridized to a separate array, for a total of ten arrays.