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Metabolic reprogramming of macrophage polarization by creatine [RNA-seq]

ABSTRACT: Metabolic reprogramming of macrophage polarization by creatine [RNA-seq]

PROVIDER: PRJNA433621 | ENA |

REPOSITORIES: ENA

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Metabolic reprogramming of macrophage polarization by creatine

Project description:Metabolic reprogramming of macrophage polarization by creatine

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Metabolic reprogramming of macrophage polarization by creatine [ATAC-seq]

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Metabolic reprogramming of macrophage polarization by creatine [ATAC-seq]

Project description:We found that the creatine metabolic pathway was differentially regulated under M1 versus M2 polarizing conditions. In return, creatine could suppress M1 by blocking STAT1 tyrosine phosphorylation while promote M2 by sustaining chromatin accessibility of specific gene loci.

2019-08-06 | GSE110403 | GEO

Metabolic reprogramming of macrophage polarization by creatine [RNA-seq]

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Cancer-derived branched-chain ketoacids modulate macrophage polarization and metabolic reprogramming

Project description:This study aims to uncover the effects of cancer-derived branched-chain ketoacids on macrophage polarization and the underlying mechanism. We uncovered the global responses of branched-chain ketoacids-stimulated macrophages by proteomics analysis. Functional enrihment analysis indicated that these ketoacids significantly altered macrophage metabolism, apoptosis and phagocytosis.

2022-10-04 | PXD032100 | Pride

High-throughput integration of metabolic and transcriptional profiles reveals major metabolic regulators of macrophage polarization

Project description:Macrophages polarize to divergent functional phenotypes depending on their microenvironment in a highly coordinated process of metabolic and transcriptional rewiring that is still poorly understood. We developed an Integrated Metabolomics and Gene Expression (IMAGE) profiling and analysis pipeline and applied it to extensively characterize global metabolic programs of macrophage polarization. IMAGE analysis identified 7 major (novel and known) regulatory modules responsible for metabolic rewiring during polarization, which we validated through extensive carbon and nitrogen labeling experiments. M1-specific modules included: inflammatory variant of the aspartate-arginosuccinate shunt; TCA cycle break at Idh expression accompanied by citrate accumulation and production of itaconate and fatty acid synthesis. In M2 macrophages we discovered significant role of glutamine in polarization, providing nitrogen for UDP-GlcNAc synthesis. Consistently, glutamine deprivation results in significant M2-specific defect in polarization. Our data provide, for the first time, a global view of the integrated transcriptional and metabolic changes that result in M1 and M2 polarization. Bone-marrow derived macrophages were generated from C57BL/6 mice were plated at ~100k cells per well in 96-well plate and stimulated with either Il4 or combination of LPS&IFNg or left unstimulated for 24 h mRNA was derived from lysates using Invitrogen oligo-dT beads

2014-05-30 | E-GEOD-53053 | biostudies-arrayexpress

Zeb1-induced metabolic reprogramming of glycolysis is essential for macrophage polarization in breast cancer

Project description:Zeb1-induced metabolic reprogramming of glycolysis is essential for macrophage polarization in breast cancer

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Metabolic reprogramming of macrophage polarization by creatine

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

2019-08-06 | GSE110456 | GEO

Branched-chain ketoacids derived from cancer cells modulate macrophage polarization and metabolic reprogramming

Project description:<p>Macrophages are prominent immune cells in the tumor microenvironment that can be educated into pro-tumoral phenotype by tumor cells to favor tumor growth and metastasis. The mechanisms that mediate a mutualistic relationship between tumor cells and macrophages remain poorly characterized. Here, we have shown <em>in vitro</em> that different human and murine cancer cell lines release branched‐chain α‐ketoacids (BCKAs) into the extracellular milieu, which influence macrophage polarization in an monocarboxylate transporter 1 (MCT1)‐dependent manner. We found that α‐ketoisocaproate (KIC) and α‐keto‐β‐methylvalerate (KMV) induced a pro‐tumoral macrophage state, whereas α‐ketoisovalerate (KIV) exerted a pro‐inflammatory effect on macrophages. This process was further investigated by a combined metabolomics/proteomics platform. KMV and KIC altered macrophage tricarboxylic acid (TCA) cycle intermediates and increased polyamine metabolism. Proteomic and pathway analyses revealed that the three BCKAs, especially KMV, exhibited divergent effects on the inflammatory signal pathways, phagocytosis, apoptosis and redox balance. These findings uncover cancer‐derived BCKAs as novel determinants for macrophage polarization with potential to be selectively exploited for optimizing antitumor immune responses.</p>

2022-10-03 | MTBLS4497 | MetaboLights

High-throughput integration of metabolic and transcriptional profiles reveals major metabolic regulators of macrophage polarization

2014-05-30 | GSE53053 | GEO

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