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Activation of GPR3-b-Arrestin2-PKM2 by DPI enhanced glycolysis in kupffer cells [single-cell RNA-seq]

ABSTRACT: Activation of GPR3-b-Arrestin2-PKM2 by DPI enhanced glycolysis in kupffer cells [single-cell RNA-seq]

PROVIDER: PRJNA773406 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16525166_1.fastq.gz	Fastqsanger.gz
	SRR16525166_2.fastq.gz	Fastqsanger.gz
	SRR16525167_1.fastq.gz	Fastqsanger.gz
	SRR16525167_2.fastq.gz	Fastqsanger.gz
	SRR16525168_1.fastq.gz	Fastqsanger.gz

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Activation of GPR3-b-Arrestin2-PKM2 by DPI enhanced glycolysis in kupffer cells

Project description:Activation of GPR3-b-Arrestin2-PKM2 by DPI enhanced glycolysis in kupffer cells

| PRJNA773400 | ENA

Activation of GPR3-b-Arrestin2-PKM2 by DPI enhanced glycolysis in kupffer cells [Human KC]

Project description:Activation of GPR3-b-Arrestin2-PKM2 by DPI enhanced glycolysis in kupffer cells [Human KC]

| PRJNA773403 | ENA

Activation of GPR3-b-Arrestin2-PKM2 by DPI enhanced glycolysis in kupffer cells [mouse KC]

Project description:Activation of GPR3-b-Arrestin2-PKM2 by DPI enhanced glycolysis in kupffer cells [mouse KC]

| PRJNA773407 | ENA

Activation of GPR3-b-Arrestin2-PKM2 by DPI enhanced glycolysis in kupffer cells [Human KC]

Project description:To investigate the human primary Kupffer cells from NAFLD patients response to DPI in vitro.

2021-10-23 | GSE186326 | GEO

Activation of GPR3-b-Arrestin2-PKM2 by DPI enhanced glycolysis in kupffer cells [mouse KC]

Project description:To investigate the transcriptional changes of Kupffer cells isolated from HFD-induced obesity mice treated with DPI in vivo.

2021-10-23 | GSE186327 | GEO

Activation of GPR3-b-Arrestin2-PKM2 by DPI enhanced glycolysis in kupffer cells [single-cell RNA-seq]

Project description:Single-cell RNAseq analysis of liver cells from NASH and cirrhosis patients has identified the presence of TREM2+ disease-associated macrophages (DAMs) in the liver that display lower expression of metabolic genes. To determine whether the DAMs are also present in patient with mild NFALD, we performed scRNAseq of freshly isolated immune cells from liver biopsies of 3 healthy donors and 3 mild NFALD patients. Kupffer cells were specifically focused.

2021-10-23 | GSE186328 | GEO

Activation of GPR3-b-Arrestin2-PKM2 by DPI enhanced glycolysis in kupffer cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-10-23 | GSE186329 | GEO

Activation of GPR3-β-arrestin2-PKM2 pathway in Kupffer cells stimulates glycolysis and inhibits obesity and liver pathogenesis.

Project description:Kupffer cells are liver resident macrophages and play critical role in fatty liver disease, yet the underlying mechanisms remain unclear. Here, we show that activation of G-protein coupled receptor 3 (GPR3) in Kupffer cells stimulates glycolysis and protects mice from obesity and fatty liver disease. GPR3 activation induces a rapid increase in glycolysis via formation of complexes between β-arrestin2 and key glycolytic enzymes as well as sustained increase in glycolysis through transcription of glycolytic genes. In mice, GPR3 activation in Kupffer cells results in enhanced glycolysis, reduced inflammation and inhibition of high-fat diet induced obesity and liver pathogenesis. In human fatty liver biopsies, GPR3 activation increases expression of glycolytic genes and reduces expression of inflammatory genes in a population of disease-associated macrophages. These findings identify GPR3 activation as a pivotal mechanism for metabolic reprogramming of Kupffer cells and as a potential approach for treating fatty liver disease.

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Lipolysis drives expression of the constitutively active receptor GPR3 to induce adipose thermogenesis [siRNAGPR3]

Project description:Thermogenic adipocytes possess a therapeutically appealing, energy-expending capacity, which is canonically cold-induced by ligand-dependent activation of b-adrenergic G protein-coupled receptors (GPCRs). Here we uncover an alternate paradigm of GPCR-mediated adipose thermogenesis through the constitutively active receptor, GPR3. We show that the N-terminus of GPR3 confers intrinsic signaling activity, resulting in continuous Gs-coupling and cAMP production without an exogenous ligand. Thus, transcriptional induction of Gpr3 represents the regulatory parallel to ligand-binding of conventional GPCRs. Consequently, increasing Gpr3 expression in thermogenic adipocytes is alone sufficient to drive energy expenditure and counteract metabolic disease in mice. Gpr3 transcription is cold-stimulated by a lipolytic signal and dietary fat potentiates GPR3-dependent thermogenesis to amplify the response to caloric excess. Moreover, we find GPR3 to be an essential, adrenergic-independent regulator of human brown adipocytes. Taken together, our findings reveal a noncanonical mechanism of GPCR control and thermogenic activation through the lipolysis-induced expression of constitutively active GPR3.

2021-04-28 | GSE173389 | GEO

Lipolysis drives expression of the constitutively active receptor GPR3 to induce adipose thermogenesis [hWA]

2021-04-28 | GSE173388 | GEO