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Glucocorticoids sensitive progenitor PDGFRα+ cells switching to white adipocytes cause visceral obese via methylation modification of

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE154091 | GEO | 2023/07/07

REPOSITORIES: GEO

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Glucocorticoids sensitive progenitor PDGFRα+ cells switching to white adipocytes cause visceral obese via methylation modification of TEAD1 (RNA-seq)

Project description:Glucocorticoids have impact on visceral obese which crucial contributor to the burden of obesity complications. Subcutaneous and visceral adipose have the heterogeneity of cellular populations. However, the mechanism of glucocorticoids mediated depot-specific regulation remains unclear. Here, we report PDGFRα+ progenitors, dominated in visceral adipose which can convert to white-typical adipocytes, are glucocorticoid-sensitive progenitors. While CD137+ progenitors, mainly harbored in subcutaneous adipose, which are beige-typical adipocytes, are glucocorticoid-passivated progenitors. Mechanistically, we proved that Glucocorticoids elevate TEAD1, transcriptional coactivator of glucocorticoid receptor, by down-regulating the methylation states in PDGFRα+ progenitors. TEAD1 bonds the accessible binding sites in miR-27b promoter region and transcriptionally increases miR-27b expression which previously proved to be the browning ability inhibitor in human and rodent white adipose. These data provide insight into the mechanism of glucocorticoids mediation of visceral obesity and the pathophysiology of depot-specific variations of high fat diet induced obesity.

2023-07-07 | GSE154090 | GEO

Glucocorticoids sensitive progenitor PDGFRα+ cells switching to white adipocytes cause visceral obese via methylation modification of TEAD1 (ATAC-seq)

2023-07-07 | GSE154089 | GEO

Glucocorticoids sensitive progenitor PDGFRα+ cells switching to white adipocytes cause visceral obese via methylation modification of TEAD1 (ChIP-seq)

2023-07-07 | GSE154088 | GEO

Glucocorticoids sensitive progenitor PDGFRα+ cells switching to white adipocytes cause visceral obese via methylation modification of TEAD1 (Bisultite-seq)

2023-07-07 | GSE154087 | GEO

Glucocorticoids sensitive progenitor PDGFRα+ cells switching to white adipocytes cause visceral obese via methylation modification of

Project description:Glucocorticoids sensitive progenitor PDGFRα+ cells switching to white adipocytes cause visceral obese via methylation modification of

| PRJNA645091 | ENA

Glucocorticoids sensitive progenitor PDGFRα+ cells switching to white adipocytes cause visceral obese via methylation modification of TEAD1 (ATAC-seq)

Project description:Glucocorticoids sensitive progenitor PDGFRα+ cells switching to white adipocytes cause visceral obese via methylation modification of TEAD1 (ATAC-seq)

| PRJNA645100 | ENA

Glucocorticoids sensitive progenitor PDGFRα+ cells switching to white adipocytes cause visceral obese via methylation modification of TEAD1 (RNA-seq)

Project description:Glucocorticoids sensitive progenitor PDGFRα+ cells switching to white adipocytes cause visceral obese via methylation modification of TEAD1 (RNA-seq)

| PRJNA645102 | ENA

Glucocorticoids sensitive progenitor PDGFRα+ cells switching to white adipocytes cause visceral obese via methylation modification of TEAD1 (Bisultite-seq)

Project description:Glucocorticoids sensitive progenitor PDGFRα+ cells switching to white adipocytes cause visceral obese via methylation modification of TEAD1 (Bisultite-seq)

| PRJNA645098 | ENA

Glucocorticoids sensitive progenitor PDGFRα+ cells switching to white adipocytes cause visceral obese via methylation modification of TEAD1 (ChIP-seq)

Project description:Glucocorticoids sensitive progenitor PDGFRα+ cells switching to white adipocytes cause visceral obese via methylation modification of TEAD1 (ChIP-seq)

| PRJNA645099 | ENA

Effects of irisin on the differentiation and browning of human visceral white adipocytes.

Project description:BACKGROUND:The aim of this study was to explore the effects of irisin on human visceral adipose tissue and adipocytes functions. METHODS:Fresh human visceral white adipose tissues derived from 11 donors were used to examine the effects of irisin on browning, adipogenesis and osteogenesis gene expression, and anti-inflammatory properties. Preadipocytes were also used to examine the effects of irisin on mitochondrial respiration, adipogenic differentiation, and osteogenic differentiation. KEY RESULTS:Irisin significantly increased cellular mitochondrial energy metabolism in differentiated visceral adipocytes. Irisin also increased mRNA levels of transcriptional regulators of brite/beige adipocytes (UCP-1, PGC1α, PRDM16, TMEM26, and CD137) in subcutaneous white adipose tissue but not in visceral/brown adipose tissue or their derived mature adipocytes. In parallel, irisin increased the protein levels of UCP-1 in subcutaneous white adipose tissue, but had no effect on the expression of this protein in visceral white adipose tissue and perirenal brown adipose tissue. However, irisin inhibited adipogenic differentiation, promoted osteogenic differentiation in visceral adipocytes, down-regulated adipogenesis, and upregulated osteogenesis genes expression in visceral fat tissue. Moreover, administration of irisin reduced the expression of proinflammatory marker mRNAs in both visceral and subcutaneous white adipose tissue. CONCLUSIONS:Our data suggest that (1) irisin may increase mitochondrial respiration and glycolysis in visceral adipocytes by a UCP-1 independent pathway; (2) irisin promotes anti-inflammatory activity on fat tissue.

| S-EPMC6943454 | biostudies-literature

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