ArticleMolecular endocrinology (Baltimore, Md.)2013
Acute genome-wide effects of rosiglitazone on PPARγ transcriptional networks in adipocytes.
Article in Molecular endocrinology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 69 citations in OpenAlex.
- The RBM14/CoAA-interacting, long intergenic non-coding RNA Paral1 regulates adipogenesis and coactivates the nuclear receptor PPARγ.Scientific reports · 2017Trial
- A transcriptional cofactor GRIP1 drives PPARγ DNA binding and p300-dependent enhancer activity during homeostatic macrophage polarization.Science advances · 2026Article
- Genome-wide chromatin profiling reveals a nonlimiting role for RXR in macrophage-like cells stimulated with multiple nuclear receptor agonists.The Journal of biological chemistry · 2026Article
- Aerobic glycolysis drives differentiation of unilocular adipocytes.Journal of lipid research · 2026Article
- Extensive enhancer crosstalk controls PPARG2 activation during adipogenesis.Nature communications · 2026Article
- Article
- Limitations in PPARα-dependent mitochondrial programming restrain the differentiation of human stem cell-derived β cells.Nature communications · 2025Article
- Structural Basis of PPARγ-Mediated Transcriptional Repression by the Covalent Inverse Agonist FX-909.Journal of medicinal chemistry · 2025Article
- Isolation and Characterization of Primary Bone Marrow Adipocytes in Rodent Models.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Agonists of the Nuclear Receptor PPARγ Can Produce Biased Signaling.Molecular pharmacology · 2024Article
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- TMEM120A/TACAN: A putative regulator of ion channels, mechanosensation, and lipid metabolism.Channels (Austin, Tex.) · 2023Review
- Simvastatin Improves Benign Prostatic Hyperplasia: Role of Peroxisome-Proliferator-Activated Receptor-γ and Classic WNT/β-Catenin Pathway.International journal of molecular sciences · 2023Article
- Regulatory Effects and Mechanism of Action of Green Tea Polyphenols on Osteogenesis and Adipogenesis in Human Adipose Tissue-Derived Stem Cells.Current issues in molecular biology · 2022Article
- PPARγ lipodystrophy mutants reveal intermolecular interactions required for enhancer activation.Nature communications · 2022Article
- Genomic loci mispositioning in Tmem120a knockout mice yields latent lipodystrophy.Nature communications · 2022Article
- Article
- Matrigel® enhances 3T3-L1 cell differentiation.Adipocyte · 2021Article
- Article
- The B56α subunit of PP2A is necessary for mesenchymal stem cell commitment to adipocyte.EMBO reports · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peroxisome proliferator-activated receptor γ (PPARγ) is a master regulator of adipocyte differentiation, and genome-wide studies indicate that it is involved in the induction of most adipocyte genes. Here we report, for the first time, the acute effects of the synthetic PPARγ agonist rosiglitazone on the transcriptional network of PPARγ in adipocytes. Treatment with rosiglitazone for 1 hour leads to acute transcriptional activation as well as repression of a number of genes as determined by genome-wide RNA polymerase II occupancy. Unlike what has been shown for many other nuclear receptors, agonist treatment does not lead to major changes in the occurrence of PPARγ binding sites. However, rosiglitazone promotes PPARγ occupancy at many preexisting sites, and this is paralleled by increased occupancy of the mediator subunit MED1. The increase in PPARγ and MED1 binding is correlated with an increase in transcription of nearby genes, indicating that rosiglitazone, in addition to activating the receptor, also promotes its association with DNA, and that this is causally linked to recruitment of mediator and activation of genes. Notably, both rosiglitazone-activated and -repressed genes are induced during adipogenesis. However, rosiglitazone-activated genes are markedly more associated with PPARγ than repressed genes and are highly dependent on PPARγ for expression in adipocytes. By contrast, repressed genes are associated with the other key adipocyte transcription factor CCAAT-enhancer binding proteinα (C/EBPα), and their expression is more dependent on C/EBPα. This suggests that the relative occupancies of PPARγ and C/EBPα are critical for whether genes will be induced or repressed by PPARγ agonist.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.