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CCR1 is a novel target in the treatment of NASH by regulating macrophage activation through mTORC1 signaling

ABSTRACT: CCR1 is a novel target in the treatment of NASH by regulating macrophage activation through mTORC1 signaling

PROVIDER: PRJNA986132 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24985084_1.fastq.gz	Fastqsanger.gz
	SRR24985084_2.fastq.gz	Fastqsanger.gz
	SRR24985085_1.fastq.gz	Fastqsanger.gz
	SRR24985085_2.fastq.gz	Fastqsanger.gz
	SRR24985086_1.fastq.gz	Fastqsanger.gz

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CCR1 is a novel target in the treatment of NASH by regulating macrophage activation through mTORC1 signaling

Project description:The number of patients with non-alcoholic steatohepatitis (NASH) is dramatically increasing globally. Recently, specific chemokine receptors have garnered interest as therapeutic targets in NASH. In different murine models with NASH, the level of CCR1 in plasma and the expression of CCR1 in liver increased, suggesting that CCR1 may be involved in the progression of NASH. Recent studies have shown that a variety of chemokines and their receptors play a certain role in the development of NASH. However, the role of CCR1 in pathogenesis of NASH remains obscure. Therefore, this study aims to explore the effect of CCR1 on the development of NASH. The results suggest that the absence of CCR1 prevents hepatic steatosis and abnormal glucose metabolism in the progression of NASH, and these results emphasize the impacts of CCR1 on macrophage recruitment and fibrosis in mice with NASH. Thus, the findings of the current study provide a new strategy for the clinical treatment of NASH.

2025-06-11 | GSE235478 | GEO

Protective Role of Macrophage Osteopontin in NASH

Project description:To study role of macrophage derived osteopontin in NASH

2023-03-31 | GSE227328 | GEO

Selective mTORC1 inhibition prevents and treats NAFLD and NASH

Project description:Selective mTORC1 inhibition prevents and treats NAFLD and NASH

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ccr1-1

Project description:Regulation of carotenoid composition and shoot branching in Arabidopsis by a chromatin modifying histone methyltransferase, SDG8<br>Comparison of transcript profiles between wild type Columbia and ccr1 (carotenoid and chloroplast regulatory) mutant, which contains a mutation in At1g77300 (SDG8)

2009-10-01 | E-MEXP-1787 | biostudies-arrayexpress

Butyrate limits inflammatory macrophage niche in NASH

Project description:Butyrate limits inflammatory macrophage niche in NASH

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Protective Role of Macrophage Osteopontin in NASH

Project description:Protective Role of Macrophage Osteopontin in NASH

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Bardoxolone methyl improves nonalcoholic steatohepatitis through inhibition of macrophage recruitment

Project description:Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease caused by excess fat accumulation, closely associated with obesity and metabolic syndrome.Bardoxolone methyl (2-Cyano-3,12-dioxooleana-1,9(11)-dien-28-oic acid methyl ester, CDDO-Me) is a potent activator of nuclear factor erythroid 2-related factor 2 (Nrf2). Some clinical trials of CDDO-Me were conducted for chronic kidney diseases and pulmonary arterial hypertension, whereas the hepatoprotective effect of CDDO-Me on nonalcoholic steatohepatitis (NASH) has not yet been elucidated. The purpose of this study was to determine the hepatoprotective potential and mechanisms of CDDO-Me in a diet-induced NASH mouse model. Whole transcriptome analysis revealed that CDDO-Me markedly inhibited the expressions of chemokine ligands, Ccl3 and Ccl4, and the chemokine receptors, Ccr1 and Ccr5 that increased in NASH mice while activating Nrf2-dependent pathway. Serum protein levels of CCL3 and CCL4 upregulated in NASH mice were inhibited in a dose-dependent manner by treatment with CDDO-Me. CDDO-Me inhibited the expression levels of Ccr1 and Ccr5, and simultaneously blocked Ccl3 and Ccl4 the ligands of the receptors, respectively in RAW264.7 cell line. Taken together with the observations, CDDO-Me directly inhibits the expression of CCL3-CCR1 and CCL4-CCR5 axes in macrophages of NASH mice, which might contribute to the improvement of nonalcoholic steatohepatitis and fibrosis through the interference of monocyte-derived macrophage migration.

2024-08-02 | GSE239861 | GEO

Rheb1-mTORC1 maintains macrophage differentiation and phagocytosis in mice

Project description:Ras homolog enriched in brain (Rheb1) is a small GTPase and is known to be a direct activator of mTORC1. Dysregulation of Rheb1 has been shown to impair the cellular-energetic state and cell homeostasis. However, the role of Rheb1 in monocytes/macrophages differentiation and maturation is not clear. Here, we investigate the role of Rheb1 in mouse myelopoiesis using a Rheb1 conditional deletion murine model. We found that the absolute number of macrophages decreased in the bone marrow (BM) of Rheb1-deficient mice. Loss of Rheb1 inhibited the monocyte-to-macrophage differentiation process. Additionally, Rheb1 deletion reduced phagocytosis ability of macrophages by inhibiting the mTORC1 signaling pathway. Furthermore, 3BDO (an activator of mTORC1) rescued the phagocytosis ability of Rheb1-deficient macrophages. Thus, Rheb1 is critical for macrophage production and phagocytosis and executes these activities possibly via mTORC1-dependent pathway.

2018-03-23 | GSE79538 | GEO

IFN-g Regulates mTORC1, Cellular Metabolism and mRNA Translation to Potentiate Inflammatory Macrophage Activation [RNA-Seq]

Project description:IFN-g primes macrophages for enhanced inflammatory activation by TLRs and microbial killing, but little is known about the regulation of cell metabolism or mRNA translation during priming. We found that IFN-g regulates macrophage metabolism and translation in an integrated manner by targeting mTORC1 and MNK pathways that converge on the selective regulator of translation initiation eIF4E. Physiological downregulation of the central metabolic regulator mTORC1 by IFN-g was associated with autophagy and translational suppression of repressors of inflammation such as HES1. Genome-wide ribosome profiling in TLR2-stimulated macrophages revealed that IFN-g selectively modulates the macrophage translatome to promote inflammation, further reprogram metabolic pathways, and modulate protein synthesis. These results add IFN-g-mediated metabolic reprogramming and translational regulation as key components of classical inflammatory macrophage activation. RPF and RNAseq libraries were generated from mock or IFN-g-primed human macrophages. Cells were stimulated with Pam3Cys and harvested at 4 hours. Libraries were generated using protocol modified from Illumina Truseq technology.

2015-06-29 | E-GEOD-66809 | biostudies-arrayexpress

IFN-g Regulates mTORC1, Cellular Metabolism and mRNA Translation to Potentiate Inflammatory Macrophage Activation [miRNA-Seq]

Project description:IFN-g primes macrophages for enhanced inflammatory activation by TLRs and microbial killing, but little is known about the regulation of cell metabolism or mRNA translation during priming. We found that IFN-g regulates macrophage metabolism and translation in an integrated manner by targeting mTORC1 and MNK pathways that converge on the selective regulator of translation initiation eIF4E. Physiological downregulation of the central metabolic regulator mTORC1 by IFN-g was associated with autophagy and translational suppression of repressors of inflammation such as HES1. Genome-wide ribosome profiling in TLR2-stimulated macrophages revealed that IFN-g selectively modulates the macrophage translatome to promote inflammation, further reprogram metabolic pathways, and modulate protein synthesis. These results add IFN-g-mediated metabolic reprogramming and translational regulation as key components of classical inflammatory macrophage activation. microRNA-seq libraries were generated from mock or IFN-g-primed human macrophages. Cells were stimulated with or without Pam3Cys and harvested at 4 hours Libraries were generated using Illumina Truseq small RNA technology.

2015-06-29 | E-GEOD-66808 | biostudies-arrayexpress

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