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M2 macrophages independently promote beige adipogenesis via blocking adipocyte Ets1

ABSTRACT: M2 macrophages independently promote beige adipogenesis via blocking adipocyte Ets1

PROVIDER: PRJNA983407 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24910860_1.fastq.gz	Fastqsanger.gz
	SRR24910860_2.fastq.gz	Fastqsanger.gz
	SRR24910861_1.fastq.gz	Fastqsanger.gz
	SRR24910861_2.fastq.gz	Fastqsanger.gz
	SRR24910862_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

M2 macrophages independently promote beige adipogenesis via blocking adipocyte Ets1

Project description:Beige adipocytes accumulates mitochondria and alleviates metabolic disorder via activating energy expenditure. Whether the opposing process of mitochondrial biogenesis and clearance are integrated regulated in beige adipocytes is beyond known. Here we show that DNA binding protein Ets1 suppresses beige adipocyte formation via bidirectional regulation of mitochondrial biogenesis and clearance. The expression level of Ets1 was down-regulated in browning adipocytes, and up-regulated in the subcutaneous fat of obese mice. Adipocyte Ets1 heterozygous knock-in mice showed suppressed beige adipocytes formation under cold stress, while the homozygous knock-in mice are cold intolerance. On the other hand, knocking out Ets1 in adipocytes enhanced energy expenditure and protect the mice from high fat diet induced metabolic disorders. Mechanical assay suggests Ets1 binds to the promoter region of mitochondria complex coding genes and autophagy related genes, transcriptionally suppresses mitochondrial biogenesis and activates its clearance. Our results indicate that Ets1 integrally regulates the balance of mitochondria generation and degradation, hence acts as a pivotal governor of mitochondria content and negatively regulates beige adipocyte formation.

2023-07-01 | GSE234879 | GEO

M2 macrophages independently promote beige adipogenesis via blocking adipocyte Ets1.

Project description:Adipose tissue macrophages can promote beige adipose thermogenesis by altering local sympathetic activity. Here, we perform sympathectomy in mice and further eradicate subcutaneous adipose macrophages and discover that these macrophages have a direct beige-promoting function that is independent of sympathetic system. We further identify adipocyte Ets1 as a vital mediator in this process. The anti-inflammatory M2 macrophages suppress Ets1 expression in adipocytes, transcriptionally activate mitochondrial biogenesis, as well as suppress mitochondrial clearance, thereby increasing the mitochondrial numbers and promoting the beiging process. Male adipocyte Ets1 knock-in mice are completely cold intolerant, whereas male mice lacking Ets1 in adipocytes show enhanced energy expenditure and are resistant to metabolic disorders caused by high-fat-diet. Our findings elucidate a direct communication between M2 macrophages and adipocytes, and uncover a function for Ets1 in responding to macrophages and negatively governing mitochondrial content and beige adipocyte formation.

| S-EPMC10883921 | biostudies-literature

TGF-b/Smad3 inhibition synergizes with PPARg agonism to reduce fibrosis and enhance functional beige adipogenesis

Project description:Adipose tissue depots vary markedly in their ability to store and metabolize triglycerides, undergo beige adipogenesis and be susceptibile to metabolic disease. The molecular mechanisms that underlie such heterogeneity are not entirely clear. Previously, we showed that TGF-b signaling regulates the browning of white adipose tissue via recruitment of dedicated beige progenitors. Here, we find that TGF-b signals dynamically regulate the balance between adipose tissue fibrosis and beige adipogenesis. Elevated basal and high-fat diet inducible activation of TGF-b/Smad3 signaling was observed in the visceral (epididymal) adipose tissue depot. Activation of TGF-b/Smad3 signaling was associated with increased adipose tissue fibrosis. RNA-seq combined with fluorescence-activated cell sorting of stromal vascular fraction of epididymal white adipose tissue depot resulted in identification of TGF-b/Smad3 regulated ITGA5+ fibrogenic progenitors. TGF-b/Smad3 signal inhibition, genetically or pharmacologically, reduced fibrosis and increased functional beige adipogenesis. TGF-b/Smad3 antagonized the beneficial effects of PPARγ , activation whereas TGF-b receptor 1 inhibition synergized with actions of rosiglitazone, a PPARγ agonist, to dampen fibrosis and promote beige adipogenesis. There was a positive correlation between TGF-b activation and levels of fibrosis marker, ITGA5, in human adipose tissue samples , with visceral (omental) adipose tissue depot exhibiting higher fibrosis potential than subcutaneous or brown adipose tissue depots. Taken together, out data provide TGF-b/Smad3 signaling operates at the nexus of adipose tissue fibrosis and functional beige adipogenesis.

2025-09-01 | GSE268791 | GEO

PdgfrB signaling alters the beige adipogenic niche

Project description:Ageing beige adipose progenitor cells overexpress platelet derived growth factor receptor beta (PdgfrB) to prevent beige adipogenesis. Genetically deleting PdgfrB in restores beige adipocyte generation whereas activating PdgfrB in juvenile mice blocks beige fat formation.

2023-03-06 | GSE226695 | GEO

Ets1 suppresses adipose beiging process via bidirectional regulation of mitochondrial biogenesis and clearance

2022-12-22 | GSE221335 | GEO

Aging impairs cold-induced beige adipogenesis and adipocyte metabolic reprogramming

Project description:Aging impairs cold-induced beige adipogenesis and adipocyte metabolic reprogramming

| PRJNA945052 | ENA

β-adrenergic signaling-regulated MYPT1-PP1β phosphatase bridges chromatin states and actomyosin-tension-mediated YAP/TAZ transcriptional network for beige adipogenesis under cold stress

Project description:Protein kinase A phosphorylates proteins including histone H3 lysine 9 (H3K9) demethylase JMJD1A to facilitate beige adipogenesis upon β-adrenergic receptor (β-AR) activation, however, phosphatase(s) that antagonizes phosphorylation to inhibit beige adipogenesis is incompletely understood. Here we show that MYPT1-PP1β is a phosphatase that negatively regulates beige adipogenesis via dephosphorylation of pS265-JMJD1A and myosin regulatory light chain. Upon β-AR activation, MYPT1-PP1β is inhibited via T694 phosphorylation of MYPT1, facilitating phosphorylation of JMJD1A and beige adipogenesis under cold stress. Depletion of MYPT1-PP1β induces Ucp1 by orchestrating JMJD1A-mediated H3K9 demethylation and actomyosin-tension mediated YAP/TAZ activation. This induction of Ucp1 is abrogated in adipocytes expressing catalytically dead JMJD1A mutant, indicating that the coordinated epigenetic and transcriptional mechanisms are essential for beige adipogenesis. We also show that preadipocytes specific Mypt1 deficient mice exhibit higher cold tolerance with higher Ucp1 levels in subcutaneous white adipose tissues compared to control mice confirming its role at animal levels.

2022-09-26 | PXD031210 | JPOST Repository

Aging impairs cold-induced beige adipogenesis and adipocyte metabolic reprogramming [single-nucleus RNA-seq]

Project description:Aging impairs cold-induced beige adipogenesis and adipocyte metabolic reprogramming [single-nucleus RNA-seq]

| PRJNA945058 | ENA

Aging impairs cold-induced beige adipogenesis and adipocyte metabolic reprogramming [single-cell RNA-seq]

Project description:Aging impairs cold-induced beige adipogenesis and adipocyte metabolic reprogramming [single-cell RNA-seq]

| PRJNA945059 | ENA

Distinct signaling and transcriptional pathways regulate peri-weaning development and cold-induced recruitment of beige adipocytes

Project description:Adipose tissue provides a defense against starvation and environmental cold. These dichotomous functions are performed by three distinct cell types: energy-storing white adipocytes, and thermogenic beige and brown adipocytes. Previous studies have demonstrated that exposure to environmental cold stimulates the recruitment of beige adipocytes in the white adipose tissue (WAT) of mice and humans, a process that has been extensively investigated. However, beige adipose tissue also develops during the peri-weaning period in mice, a developmental program that remains poorly understood. Here, we address this gap in our knowledge using genetic, imaging, physiologic, and genomic approaches. We find that, unlike cold-induced recruitment in adult animals, peri-weaning development of beige adipocytes occurs in a temperature- and sympathetic nerve-independent manner. Instead, the transcription factor B cell leukemia/lymphoma 6 (BCL6) acts in a cell autonomous manner to regulate the commitment but not the maintenance phase of beige adipogenesis. Genome-wide RNA-seq studies reveal that BCL6 regulates a core set of genes involved in fatty acid oxidation and mitochondrial uncoupling, which are necessary for development of functional beige adipocytes. Together, our findings demonstrate that distinct transcriptional and signaling mechanisms control peri-weaning development and cold-induced recruitment of beige adipocytes in mammals.

2020-03-02 | GSE140259 | GEO

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