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Propagation of Adipogenic Signals through an Epigenomic Transition State

ABSTRACT: The transcriptional mechanisms by which temporary exposure to developmental signals instigates adipocyte differentiation are unknown. During early adipogenesis, we find transient enrichment of the glucocorticoid receptor (GR), CCAAT/enhancer binding protein b (CEBPb), p300, mediator subunit 1, and histone H3 acetylation near genes involved in cell proliferation, development and differentiation, including the gene encoding the master regulator of adipocyte differentiation, peroxisome proliferator activated receptor g2 (PPARg2). Occupancy and enhancer function are triggered by adipogenic signals, and diminish upon their removal. GR, which is required for adipogenesis but need not be active in the mature adipocyte, transiently functions with other enhancer proteins to propagate a new program of gene expression that includes induction of PPARg2, thereby providing a memory of the earlier adipogenic signal. Thus, the conversion of preadipocyte to adipocytes involves the formation of an epigenomic transition state that is not observed in cells at the beginning or end of the differentiation process.

ORGANISM(S): Mus musculus

PROVIDER: GSE21898 | GEO | 2010/05/20

SECONDARY ACCESSION(S): PRJNA126859

REPOSITORIES: GEO

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Project description:Background: Obesity is characterized as a disease that directly affects the whole-body metabolism and is associated with excess fat mass and several related comorbidities. Dynamics of the adipocyte hypertrophy and hyperplasia play an important role in health and disease, especially in obesity. Human adipose-derived stem cells (hASC) represent an important source for understanding the entire adipogenic differentiation process. However, little is known about the triggering step of adipogenesis in hASC. Here, we performed a proteogenomic approach for understanding the protein abundance alterations expression changes during the initiation of the adipogenic differentiation process. Methods: hASC were isolated from adipose tissue from three donors, characterized and expanded. Cells were cultured for 24 hours in adipogenic differentiation medium followed to protein extraction. We used shotgun proteomics to compare the proteomic profile of 24h-adipogenic differentiated and undifferentiated hASC. Besides, we used our previously next-generation sequencing data (RNA-seq) from the total and polysomal mRNA fractions of hASC to study post-transcriptional regulation during the initial steps of adipogenesis. Results: We identified a total of 3,.420 proteins out of and 48,.336 peptides, being 92 exclusively identified proteins in the undifferentiated hASC and 53 exclusive proteins in 24h-differentiated cells. Using a stringent criterion, we identified 33 differentially abundant proteins when compare 24h-differentiated versus undifferentiated hASC (14 upregulated and 19 downregulated, respectively). Among the upregulated proteins, we shortlist identified several adipogenic-related proteins. Combined analysis of the proteome and the transcriptome allowed the identification of positive correlation coefficients between proteins and mRNAs. Conclusions: These results demonstrate a specific proteome profile related to adipogenesis at the very beginning (24h) of the differentiation process in hASC, which represents an important piece for a better understanding of human adipogenesis and obesity. In addition, the adipogenic differentiation is fine-tuning regulated at transcriptional, post-transcriptional and post-translational levels.

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Propagation of Adipogenic Signals through an Epigenomic Transition State

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