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

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

PROVIDER: PRJNA645098 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12183800_1.fastq.gz	Fastqsanger.gz
	SRR12183800_2.fastq.gz	Fastqsanger.gz
	SRR12183799_1.fastq.gz	Fastqsanger.gz
	SRR12183799_2.fastq.gz	Fastqsanger.gz

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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.

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Project description:summary: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.

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PDGFRα+ not CD137+ progenitors control visceral obesity via glucocorticoid mediated TEAD1 methylation state

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