Similar Datasets
Project description:Fto knockdown in 2-day post-confluent 3T3-L1 preadipocytes
| PRJNA454285 | ENA
Project description:Excessive fat accumulation is a major risk factor for the development of type 2 diabetes.To determine the mechanisms by wich TP53INP2 regulates adipogenesis, gene expression profile was performed in TP53INP2-deficient 3T3-L1 cells at different stages of differentiation.
2018-04-03 | GSE93637 | GEO
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.
2013-12-31 | GSE25423 | GEO
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: [1] 3T3-L1 preadipocytes (passage 19) transfected with a control scrambled siRNA at 24h after transfection (siC.24h), [2] 3T3-L1 preadipocytes (p.19) transfected with a siRNA directed against LSD1 at 24h after transfection (siLsd1.24h), [3] 3T3-L1 preadipocytes (p.21) transfected with a control scrambled siRNA at 48h after transfection (siC.48h), and [4] 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.
2013-12-31 | E-GEOD-25423 | biostudies-arrayexpress
Project description:Cistanche deserticola Ma (cistanche) is a traditional herb with a wide range of therapeutic properties. However, no evidence of cistanche's effect on adipogenesis has been found. The effect of cistanche that promotes the adipogenesis of 3T3-L1 preadipocytes was proved by using MTT spectrophotometry, Nile Red staining, Oil Red O staining and transcriptome sequencing technology. The mRNA level of key transcription factors for adipogenesis such as PPAR, AP2 and LPL were examined by RT-PCR. The results showed that the intracellular lipid content in cistanche treated cells were notably increased when compared with the non-treated cells. Between the differentiation and cistanche treated groups, the expression of adipogenesis related genes such as grow hormone releasing hormone (Ghrp), BCL2/adenovirus E1B interacting protein 3 (Bnip3) and Gastric inhibitory polypeptide receptor (Gipr) were significantly increased. Our findings also verified that cistanche promoted adipogenesis, which was accompanied by up-regulated level of Bnip3 and PPAR. This study could uncover new signaling pathways involved in adipogenesis regulation.
| S-EPMC8887766 | biostudies-literature
Project description:3T3-L1 preadipocytes were treated with control siRNA and two siRNA to FTO: siFTO-1 and siFTO-2. 24 hours after transfection, cells were induced to differentiation with MDI cocktail. RNA were collected from non-treated cells, and those treated with control siRNA, siFTO-1 or siFTO-2 at 0, 6, 24 and 72 hours post induction. Three replicates were done for each data point.
2015-05-29 | GSE69313 | GEO
Project description:Obesity is an energy balance disorder in which nutrient intake chronically exceeds energy expenditure, resulting in the accumulation of white adipose tissue. Increased adiposity is due to increases in the number and size of adipocytes, which leads to increased body fat and metabolic consequences. Adipocytes induce insulin resistance by promoting lipotoxicity and modulating adipokine secretion. Therefore, a thorough understanding of the mechanisms that regulate adipogenesis could have clinical relevance in preventing and treating obesity and the metabolic syndrome. In this study, we performed miRNA array to measure miRNA profiles of undifferentiated and differentiated 3T3-L1 adipocytes using Agilent(r) miRNA array. We show that miRNA profile changes during adipogenesis. Thus, this data would be useful to find the distinct role of miRNAs for the regulation of adipogenesis.
2013-08-07 | E-MTAB-1783 | biostudies-arrayexpress
Project description:Enhancer activation is essential for cell-type specific gene expression during cellular differentiation, however, how enhancers transition from a hypoacetylated “primed” state to a hyperacetylated-active state is incompletely understood. Here, we show SET domain-containing 5 (SETD5) forms a complex with NCoR-HDAC3 co-repressor that prevents histone acetylation of enhancers for two master adipogenic regulatory genes Cebpa and Pparg early during adipogenesis. The loss of SETD5 from the complex is followed by enhancer hyperacetylation. SETD5 protein levels were transiently increased and rapidly degraded prior to enhancer activation providing a mechanism for the loss of SETD5 during the transition. We show that induction of the CDC20 co-activator of the ubiquitin ligase leads to APC/C mediated degradation of SETD5 during the transition and this operates as a molecular switch that facilitates adipogenesis.
2021-10-25 | GSE183846 | GEO
Project description:The objective of this analysis was to identify the genes that are differentially expressed between preadipocytes with low or high adipogenic capability
2017-01-03 | GSE90580 | GEO
Project description:Adipocytes play a critical role in metabolic homeostasis. Here we report that Zbtb9 acts as a positive regulator of PPARγ transcriptional activity in 3T3-L1 mature adipocytes, and PPARγ target gene expression was decreased when Zbtb9 deficiency was induced by shRNA-mediated knockdown (KD), establishing Zbtb9 as a newly identified PPARγ cofactor. Given the central role of PPARγ in adipogenesis, we also sought to investigate the role of Zbtb9 in adipogenesis in 3T3-L1 cells. Surprisingly, lipid droplet formation was significantly increased in Zbtb9 KD cells compared with the control, as was the expression of adipogenic genes including Pparg, Adipoq, Fabp4, and Cd36. The transcriptome of Zbtb9-KD fibroblasts, prior to the initiation of differentiation showed that the E2F targets pathway was significantly upregulated compared to the control cells. In addition, E2F activity was increased in Zbtb9-KD fibroblasts using luciferase reporter assay. Accordingly, RB phosphorylation was enhanced in Zbtb9-KD cells. Collectively, these results demonstrate that Zbtb9 inhibits adipogenesis as a negative regulator of Pparg expression via altered pRB-E2F1 signaling. Together, our findings revealed complex cell-state dependent roles of Zbtb9 in adipocytes, identifying a new molecule that may be important in the pathogenesis and treatment of obesity and T2D.
2024-11-14 | GSE253544 | GEO