Project description:In our earlier study, it was shown that Rosiglitazone enhances the brown adipogenesis of Immortalized Human Bone Marrow Mesenchymal Stromal Cells - hTERT (iMSC3). The current study compared the transcriptomics profiles of the different adipocytes derived from iMSC3 reported in our previous study. The complete transcriptomic profiles of iMSCs and adipocytes differentiated with and without Rosiglitazone treatment revealed a set of marker genes that warrant further investigation. The transcriptomics analysis revealed the upregulation and uniquely expression of genes due to Rosiglitazone treatment seems to have roles in brown adipogenesis.
Project description:Human multipotent adipose-derived stem (hMADS) cells are differentiated in white or brown adipocytes with Rosiglitazone between days 14 and 18. PPAR alpha was silenced by siRNA transfections at day 10.
Project description:SGBS cells were used as a model system to investigate the cellular mode of action of a variety of plasticizers in human adipocytes. In brief, cells were cultured at 5% CO2 and 37°C in 95% humidity. Cells of generation 40 and passage 3 after thawing were grown to confluence with DMEM/F12 containing 33 µM biotin, 17 µM pantothenate, 100 U/l penicillin, and 0.1 mg/l streptomycin (basal medium) supplemented with 10% FCS (Gibco, Carlsbad, CA, USA). According to the standard differentiation protocol, differentiation was initiated (day 0) after changing to serum-free basal medium supplemented with 0.1 μM cortisol, 0.01 mg/ml apo-transferrin, 0.2 nM triiodothyronine, and 20 nM human insulin (differentiation medium) with the addition of 2 µM rosiglitazone, 25 nM dexamethasone, and 200 µM 3-isobutyl-1-methylxanthine for the first four days. The positive control was differentiated using the standard protocol with rosiglitazone. For plasticizer treatments, differentiation was conducted without rosiglitazone and cells were continuously exposed from day 0 – day 16 to the plasticizers or their transformation products. As for plasticizer treatments, the negative control was differentiated with rosiglitazone-free medium containing equivalent amounts of solvent (0.01 MeOH, v/v) for 16 days, resulting in minimal differentiation. All media were renewed every second day to mimic continuous exposure.
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
Project description:Here, we evaluated the molecular effects of MINCH exposure, as primary metabolite of the DEHP substitute DINCH, on the proteome of differentiating SGBS adipocytes. This study includes data on rosiglitazone differentiated controls, 10 µM MINCH exposure, and exposure to the selective PPAR inhibitor GW9662, as well as combinations thereof.
Project description:Here, we evaluated the molecular effects of MINCH exposure, as primary metabolite of the DEHP substitute DINCH, on the acetylome profiles of differentiating SGBS adipocytes. This study includes data on rosiglitazone differentiated controls, 10 µM MINCH exposure, and exposure to the selective PPAR inhibitor GW9662, as well as combinations thereof.
Project description:Here, we evaluated the molecular effects of MINCH exposure, as primary metabolite of the DEHP substitute DINCH, on the phosphoproteome profiles of differentiating SGBS adipocytes. This study includes data on rosiglitazone differentiated controls, 10 µM MINCH exposure, and exposure to the selective PPAR inhibitor GW9662, as well as combinations thereof.
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
Project description:This study aimed at determining the transcriptional changes associated with the white-to-brown conversion of human mesenchymal adipose-derived stem cells firstly differentiated into white adipocytes (in the presence of rosiglitazone from day 2 to day 9). White differentiation was completed within 14 days, and PPARg (rosiglitazone) or PPARa (GW7647) agonists were added to the medium for 4 additional days to induce the brown phenotype. Cells were harvested at day 18 and processed for microarray experiments (Agilent).
