Microarray analysis of adipocyte co-culture with SKOv3ip1 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE104237 | GEO | 2018/05/09
REPOSITORIES: GEO
Similar Datasets
Project description:Microarray analysis of adipocyte co-culture with SKOv3ip1 cells
| PRJNA412102 | ENA
Project description:Primary human omental adipocytes were isolated from patients with non-cancer conditions. Subsequently, gene expression profiled in adipocytes and ovarian cancer cell line (SKOV3ip1) alone (control) or under co-culture conditions. Following co-culture cells were separated and total RNA isolated for microarray analysis.
2023-07-24 | GSE235641 | GEO
Project description:The hypothesis tested is that IRF3 regulates adipogenesis and adipocyte function. Global gene expression of IRF3 wildtype (WT) and knockout (KO) adipocytes at different days during differentiation was compared. The results provide evidence on how IRF3 controls PPARg -regulated adipogenic program thereby regulate adipocyte differentiation.
2021-04-22 | GSE172491 | GEO
Project description:The study investigated the interaction between omental adipocytes and OvCa cells, as a follow up to preliminary data indicating this leads to reprograming of metabolic (especially lipid) profiles in both adipocytes and OvCa cells as ovarian cancer cells (OvCa) readily metastasize to the omental fat pad in the abdomen and stimulate the release of fatty acids. In order to mimic the interaction between OvCa and omental adipocytes during metastasis, a coculture system was used that employed OvCa cells and primary human adipocytes isolated from omentum. Human primary adipocytes were isolated from omental explants from patients undergoing surgery for benign conditions. After surgical removal, omental tissue was digested with collagenase I, and primary cultures of adipocytes were established, characterized, and incorporated into the co-culture. The primary adipocytes were isolated and co-cultured with the OvCa cell line Skov3ip1. In this current submission, the the samples will be collected at 4, 18 and 24 hour time points post co-culture to determine the time dependent effect on lipid mediators, including oxylipins and ceramides. The study results included in this DRCC submission were the 18 hour time point data for oxylipins and ceramides from targeted metabolomic analysis of lipid mediators performed by the Newman lab.
2014-07-24 | ST000096 | MetabolomicsWorkbench
Project description:We sought to compare mRNA expression profiles between the parental SKOV3ip1 and taxane-resistant SKOV3TRip2 in order to determine what genes are mediating taxane resistance
2011-01-01 | GSE23779 | GEO
Project description:FACS-purified adipocyte progenitors from murine subcutaneous adipose tissue were cultured under conditions promoting general adipogenic differentiation or beige/brite adipocyte differentiation (treatment with cPGI2). Time course expression profiling was performed during differentiation. In addition, some cultures of differentiated adipocytes were stimulated with norepinephrine for 3 hours. In parallel, differentiation and norepinephrine stimulation of progenitors from interscapular brown fat was performed and profiled.
2015-08-20 | E-MTAB-3693 | biostudies-arrayexpress
Project description:The diverse transcriptional mechanisms governing cellular differentiation and development of mammalian tissue remains poorly understood. Here we report that TAF7L, a paralogue of TFIID subunit TAF7, is enriched in adipocytes and mouse white fat tissue (WAT). Depletion of TAF7L reduced adipocyte-specific gene expression and compromised adipocyte differentiation as well as WAT development. Ectopic expression of TAF7L in myoblasts reprograms these muscle precursors into adipocytes upon induction. Genome-wide mRNA-seq expression profiling and ChIP-seq binding studies confirmed that TAF7L is required for activating adipocyte-specific genes via a dual mechanism wherein it interacts with PPARM-NM-3 at enhancers and TBP/Pol II at core promoters. In vitro binding studies confirmed that TAF7L forms complexes with both TBP and PPARM-NM-3. These findings suggest that TAF7L plays an integral role in adipocyte gene expression by targeting enhancers as a cofactor for PPARM-NM-3 and promoters as a component of the core transcriptional machinery. Genome-wide mapping of TAF7L and additional factors, and mRNA-seq expression profiling prior to and following mouse adipocyte differentiation.
2013-01-07 | E-GEOD-41937 | biostudies-arrayexpress
Project description:Tight control of gene expression networks involved in adipose tissue formation and plasticity is required to adapt to energy needs and environmental cues. However, little is known about the mechanisms that orchestrate the dramatic transcriptional changes leading to adipocyte differentiation. We investigated the regulation of nascent transcription by SUMO during adipocyte differentiation using SLAMseq and ChIPseq. We discovered that SUMO has a dual function in differentiation; it supports the initial downregulation of pre-adipocyte-specific genes, while it promotes the establishment of the mature adipocyte transcriptional program. By characterizing SUMOylome dynamics in differentiating adipocytes by mass spectrometry, we found that SUMOylation of specific transcription factors like PPARG/RXR and chromatin modifiers promotes the transcription of adipogenic genes. Our data demonstrate that the sumoylation pathway helps coordinates the rewiring of transcriptional networks required for formation of functional adipocytes.
2022-02-18 | PXD024144 | Pride
Project description:Non-shivering thermogenesis in adipocytes is mediated by brown adipose tissue, purportedly through the sole action of uncoupling protein 1 (UCP1). The physiological relevance of UCP1-dependent thermogenesis has primarily been inferred from the attenuation of thermogenic output of mice genetically lacking Ucp1 from birth (germline Ucp1-/-). However, germline Ucp1-/- mice harbor secondary changes within brown adipose tissue beyond UCP1, such as reduced electron transport chain abundance. We show here that these secondary changes also encompass reduced expression of genes regulating fuel liberation, changes that would attenuate the capacity of any thermogenic pathway. Therefore, the quantitative contribution of UCP1-dependent and -independent thermogenesis is not fully understood. To mitigate the potentially confounding ancillary changes to brown adipose tissue of germline Ucp1-/- mice, we constructed mice with inducible adipocyte-selective disruption of Ucp1. We find that, while germline Ucp1-/- mice succumb to cold-induced hypothermia with complete penetrance, most mice with inducible deletion of Ucp1 maintain homeothermy in the cold. However, inducible adipocyte-selective co-deletion of Ucp1 and creatine kinase B (Ckb, an effector of UCP1-independent thermogenesis) exacerbates cold-intolerance, indicative of a negative genetic interaction and thus a parallel thermogenic function. We find no evidence for impairments in insulation or non-shivering thermogenesis in skeletal muscle that would drive this phenotype. Furthermore, following UCP1 deletion or UCP1/CKB co-deletion from mature adipocytes, moderate cold exposure triggers the regeneration of mature adipocytes that coordinately restore UCP1 and CKB to brown adipose tissue, providing further evidence of their parallel thermogenic relationship. Our findings suggest that thermogenic adipocytes utilize non-paralogous protein redundancy – through UCP1 and CKB – to promote cold-induced energy dissipation.
2024-01-10 | PXD047841 | Pride
Project description:Energy-storing white adipocytes maintain their identity by suppressing the gene program defining energy-burning thermogenic brown/beige adipocytes. Here, we reveal that the protein-protein interaction between the transcriptional co-regulator ZFP423 and brown/beige cell determination factor, EBF2, is essential for restraining the thermogenic phenotype of white adipose tissue (WAT). Disruption of the ZFP423-EBF2 protein interaction through CRISPR-Cas9 gene editing triggers widespread “browning” of WAT in adult mice. Mechanistically, adipocyte Zfp423 deficiency induces an EBF2 NuRD-to-BAF co-regulator switch and a shift in PPARgamma occupancy to thermogenic genes. This shift in PPARgamma occupancy increases the anti-diabetic efficacy of the PPARgamma agonist rosiglitazone in obesity while diminishing the unwanted weight-gaining effect of the drug. These data indicate that ZFP423 controls EBF2 co-activator recruitment and PPARgamma occupancy to determine the thermogenic plasticity of adipocytes and raise the concept of targeting transcriptional brakes in adipocyte gene expression as a therapeutic strategy to induce thermogenic adipocyte biogenesis in obesity.
2022-05-01 | GSE175654 | GEO