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Effect of time-course forskolin (FSK) treatment versus rosiglitazone (Rosi) treatment on the chromatin accessibility landscape in a new immortalized mouse adipocyte progenitor (MAP) cell line (ATAC-Seq).

ABSTRACT: To investigate how the chromatin accessibility landscape is altered during biphasic FSK-induced browning in comparison with single-phase Rosi-induced browning, We performed chromatin lanscape profiling using the nuclei sorted from MAP cells treated with vehicle (Control) or with FSK for mulitple time durations (4 hours, 1 day, or 3 days) or with Rosi for 3 days.

ORGANISM(S): Mus musculus

PROVIDER: GSE214597 | GEO | 2022/10/08

REPOSITORIES: GEO

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Effect of time-course forskolin (FSK) treatment versus rosiglitazone (Rosi) treatment on gene expression in a new immortalized mouse adipocyte progenitor (MAP) cell line (RNA-Seq).

Project description:To characterize biphasic adipocyte browning induced by chronic FSK treatment and compare this process to Rosi-induced browning, We performed gene expression profiling using MAP cells treated with vehicle or with FSK for mulitple time durations (4h, 1D, and 3D) or with Rosi for 3D.

2022-10-08 | GSE214596 | GEO

Effect of time-course forskolin (FSK) treatment versus rosiglitazone (Rosi) treatment on the chromatin accessibility landscape in a new immortalized mouse adipocyte progenitor (MAP) cell line

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Effect of time-course forskolin (FSK) treatment versus rosiglitazone (Rosi) treatment on gene expression in a new immortalized mouse adipocyte progenitor (MAP) cell line (RNA-Seq).

Project description:Effect of time-course forskolin (FSK) treatment versus rosiglitazone (Rosi) treatment on gene expression in a new immortalized mouse adipocyte progenitor (MAP) cell line (RNA-Seq).

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Differentiation of human monocytes to macrophages in the presence of GM-CSF +/- forskolin (FSK)

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Effect of time-course forskolin (FSK) treatment versus rosiglitazone (Rosi) treatment on the chromatin accessibility landscape in a new immortalized mouse adipocyte progenitor (MAP) cell line (ATAC-Seq).

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Rosiglitazone Treatment Reduces Diabetic Neuropathy in STZ treated DBA/2J mice

Project description:Diabetic Neuropathy (DN) is a common complication of diabetes. Currently, there is no drug treatment to prevent or slow the development of DN. Rosiglitazone (Rosi) is a potent insulin sensitizer and may also slow the development of DN by a mechanism independent of its effect on hyperglycemia. A two by two design was used to test the effect of Rosi treatment on the development of DN. Streptozotocin-induced diabetic DBA/2J mice were treated with Rosi. DN and oxidative stress were quantified, and gene expression was profiled using the Affymetrix Mouse Genome 430 2.0 microarray platform. An informatics approach identified key regulatory elements activated by Rosi. Diabetic DBA/2J mice developed severe hyperglycemia, DN and elevated oxidative stress. Rosi treatment did not affect hyperglycemia but did reduce oxidative stress and prevented development of thermal hypoalgesia. Two novel transcription factor binding modules were identified that may control genes correlated to changes in DN following Rosi treatment: SP1F_ZBPF and EGRF_EGRF. Rosi treatment reduced oxidative stress and DN independent of its insulin sensitizing effects. Gene expression profiling identified two novel targets activated by Rosi treatment. These targets may be useful in designing drugs with the same efficacy as Rosi in treating DN but with fewer undesirable effects. Keywords: disease and treatment analysis

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Differentiation of human monocytes to macrophages in the presence of GM-CSF +/- forskolin (FSK)

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Effect of time-course forskolin (FSK) treatment versus rosiglitazone (Rosi) treatment on the chromatin accessibility landscape in a new immortalized mouse adipocyte progenitor (MAP) cell line

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-10-08 | GSE214598 | GEO

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Antidiabetic Rosiglitazone Remodels the Adipocyte Transcriptome by Redistributing Transcription to PPARg-Driven Enhancers [HTS]

Project description:Rosiglitazone (rosi) is a powerful insulin sensitizer, but serious toxicities have curtailed its widespread clinical use. Rosi functions as a high-affinity ligand for PPARg, the adipocyte-predominant nuclear receptor (NR). The classic model, involving binding of ligand to the NR on DNA, explains positive regulation of gene expression, but ligand-dependent repression is not well understood. We have now addressed this issue by studying the direct effects of rosiglitazone on gene transcription, using global run-on sequencing (GRO-seq). Rosi-induced changes in gene body transcription were pronounced after 10 minutes and correlated with steady-state mRNA levels as well as with transcription at nearby enhancers (eRNAs). Upregulated eRNAs occurred almost exclusively at PPARg binding sites, to which rosi treatment recruited the coactivator MED1. By contrast, transcriptional repression by rosi involved a loss of MED1 from eRNA sites devoid of PPARg and enriched for other TFs including AP-1 factors and C/EBPs. Thus, rosi activates and represses transcription by fundamentally different mechanisms that could inform the future development of antidiabetic drugs.

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