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The miR-182-5p/FGF21/acetylcholine axis mediates the crosstalk between adipocytes and macrophages to promote beige fat thermogenesis

ABSTRACT: The miR-182-5p/FGF21/acetylcholine axis mediates the crosstalk between adipocytes and macrophages to promote beige fat thermogenesis

PROVIDER: PRJNA741665 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14919185.fastq.gz	Fastqsanger.gz
	SRR14919186.fastq.gz	Fastqsanger.gz
	SRR14919187.fastq.gz	Fastqsanger.gz
	SRR14919188.fastq.gz	Fastqsanger.gz
	SRR14919189.fastq.gz	Fastqsanger.gz

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The miR-182-5p/FGF21/acetylcholine axis mediates the crosstalk between adipocytes and macrophages to promote beige fat thermogenesis

Project description:The miR-182-5p/FGF21/acetylcholine axis mediates the crosstalk between adipocytes and macrophages to promote beige fat thermogenesis miR182 overexpression in primary cultured iWAT

2021-10-13 | GSE178952 | GEO

The miR-182-5p/FGF21/acetylcholine axis mediates the crosstalk between adipocytes and macrophages to promote beige fat thermogenesis.

Project description:A dynamically regulated microenvironment, which is mediated by crosstalk between adipocytes and neighboring cells, is critical for adipose tissue homeostasis and function. However, information on key molecules and/or signaling pathways regulating the crosstalk remains limited. In this study, we identify adipocyte miRNA-182-5p (miR-182-5p) as a crucial antiobesity molecule that stimulated beige fat thermogenesis by promoting the crosstalk between adipocytes and macrophages. miR-182-5p was highly enriched in thermogenic adipocytes, and its expression was markedly stimulated by cold exposure in mice. In contrast, miR-182-5p expression was significantly reduced in adipose tissues of obese humans and mice. Knockout of miR-185-5p decreased cold-induced beige fat thermogenesis whereas overexpression of miR-185-5p increased beiging and thermogenesis in mice. Mechanistically, miR-182-5p promoted FGF21 expression and secretion in adipocytes by suppressing nuclear receptor subfamily 1 group D member 1 (Nr1d1) at 5'-UTR, which in turn stimulates acetylcholine synthesis and release in macrophages. Increased acetylcholine expression activated the nicotine acetylcholine receptor in adipocytes, which stimulated PKA signaling and consequent thermogenic gene expression. Our study reveals a key role of the miR-182-5p/FGF21/acetylcholine/acetylcholine receptor axis that mediates the crosstalk between adipocytes and macrophages to promote beige fat thermogenesis. Activation of the miR-182-5p-induced signaling pathway in adipose tissue may be an effective approach to ameliorate obesity and associated metabolic diseases.

| S-EPMC8492300 | biostudies-literature

The Histone Methyltransferase SUV420H2 Regulates Brown and Beige Adipocyte Thermogenesis

Project description:Activation of brown adipose tissue (BAT) thermogenesis increases energy expenditure and alleviates obesity. Epigenetic regulation has emerged as a key mechanism underlying BAT development and function. To study the epigenetic regulation of BAT thermogenesis, we surveyed the expression of epigenetic enzymes that catalyze histone modifications in developmental beige adipocytes and found a unique expression pattern of suppressor of variegation 4-20 homolog 2 (Drosophila) (Suv420h2), a histone methyltransferase that preferentially catalyzes the tri-methylation at histone H4 lysine 20 (H4K20me3), a hallmark of gene silencing. Here we discovered that Suv420h2 expression parallels that of UCP1 expression in brown and beige adipocytes and that SUV420H2 knockdown significantly reduces, whereas SUV420H2 overexpression significantly increases UCP1 levels in brown adipocytes. Suv420h2 knockout (H2KO mice exhibit impaired cold-induced thermogenesis and are prone to diet-induced obesity. In contrast, mice with specific overexpression of Suv420h2 in adipocytes display enhanced cold-induced thermogenesis and are resistant to diet-induced obesity. Further study showed that Suv420h2 catalyzes H4K20 trimethylation at eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) promoter, leading to down-regulated expression of 4E-BP1, a negative regulator of the translation initiation complex. This in turn up-regulates PGC1α protein levels, which is associated with increased expression of thermogenic program. We conclude that Suv420h2 is a key regulator of brown/beige adipocyte development and thermogenesis.

2024-05-09 | GSE244457 | GEO

Bulk RNA sequencing of acetylcholine-synthesizing macrophages from subcutaneous adipose tissue

Project description:We aimed to study the transcriptomic profile of acetylcholine-synthesizing adipose macrophages. Using a ChAT-eGFP reporter mouse (ChAT, or choline acetyltransferase, is the main enzyme for acetylcholine biosynthesis) acutely exposed to cold temperature, we used FACS to isolate ChAT-eGFP+ and ChAT-eGFP- macrophages from inguinal subcutaneous white adipose tissue (IWAT). We subjected these cells to bulk RNA-seq to better understand the transcriptomic landscape of cholinergic macrophages under cold stress and their role in beige fat thermogenesis.

2021-07-29 | GSE174345 | GEO

The Histone Methyltransferase SUV420H2 Regulates Brown and Beige Adipocyte Thermogenesis (ATAC-Seq)

2024-05-09 | GSE245509 | GEO

Naa10p Inhibits Beige Adipocyte-mediated Thermogenesis through N-alpha-acetylation of Pgc1-alpha

Project description:We report that both conventional and adipose-specific Naa10p deletions in mice result in increased energy expenditure, thermogenesis, beige adipocyte differentiation and activation. Mechanistically, Naa10p acetylates the N-terminus of Pgc1-alpha and prevents it from interacting with Ppar[gamma] to activate key genes, such as Ucp1, involved in beige adipocyte function.

2019-08-15 | GSE133726 | GEO

Naa10p Inhibits Beige Adipocyte-mediated Thermogenesis through N-α-acetylation of Pgc1α

Project description:We reported that both conventional and adipose-specific Naa10p deletions in mice result in increased energy expenditure, thermogenesis, beige adipocyte differentiation and activation. Mechanistically, Naa10p acetylates the N-terminus of Pgc1α and prevents it from interacting with Ppar to activate key genes, such as Ucp1, involved in beige adipocyte function. We used microarrays to profile the gene expression changes by Naa10p KO in inguinal white adipose tissues (iWATs) derived from mice fed with high fat diet for 15 weeks.

2019-08-16 | GSE133865 | GEO

A novel GPR120-dependent pathway of control brown fat activation mediated by FGF21

Project description:Brown adipose tissue (BAT) thermogenesis and the browning of white adipose tissue are important components of energy expenditure. An RNAseq-based analysis of the mouse BAT transcriptome led us to identify GPR120 as a gene induced by thermogenic activation. GPR120, a G protein-coupled receptor binding unsaturated long-chain fatty acids, is known to mediate some beneficial metabolic actions of polyunsaturated fatty acids. We show that pharmacological activation of GPR120 induces BAT activity and promotes the browning of white fat in mice, whereas GRP120-null mice show impaired browning in response to cold. n-3 polyunsaturated fatty acids induce brown and beige adipocyte differentiation and thermogenic activation, and these effects require GPR120. GPR120 activation induces the release of fibroblast growth factor-21 (FGF-21) by brown and beige adipocytes and increases blood FGF21 levels. The effects of GPR120 activation are impaired in FGF21-null mice and cells. Thus, the lipid sensor GPR120 constitutes a novel pathway of brown fat activation and involves FGF21.

2016-12-12 | GSE77534 | GEO

The Histone Methyltransferase SUV420H2 Regulates Brown and Beige Adipocyte Thermogenesis

Project description:The Histone Methyltransferase SUV420H2 Regulates Brown and Beige Adipocyte Thermogenesis

| PRJNA1023212 | ENA

RNA-sequencing of Control and TLE3-deficient Beige Adipocytes

Project description:Prolonged cold exposure stimulates the recruitment of beige adipocytes within white adipose tissue. Beige adipocytes depend on mitochondrial oxidative phosphorylation to drive thermogenesis. The transcriptional coregulator TLE3 inhibits mitochondrial and metabolic gene expression in beige adipocytes.

2019-05-23 | GSE116894 | GEO

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