Primary monocyte to macrophage differentiation involves significant changes in chromosome conformation different from cultured THP-1 cells
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PROVIDER: PRJEB34069 | ENA |
REPOSITORIES: ENA
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Project description:Primary monocyte to macrophage differentiation involves significant changes in chromosome conformation different from cultured THP-1 cells
| PRJEB34065 | ENA
Project description:Use human native monocyte and induce to macrophae by GM-CSF, reserach the chromatin conformation of these two cell types.
2021-02-23 | E-MTAB-8262 | biostudies-arrayexpress
Project description:Use human native monocyte and induce to macrophae by GM-CSF, research the gene expression of these two cell types.
2021-02-23 | E-MTAB-8261 | biostudies-arrayexpress
Project description:Transcriptional profiling of Monocyte-like THP-1 Cells with Trichosporon asahii Infected THP-1 Cells comparing untreated THP-1 cells
2012-11-03 | GSE41983 | GEO
Project description:Transcriptional profiling of Monocyte-like THP-1 Cells with Trichosporon asahii Infected THP-1 Cells comparing untreated THP-1 cells Two-condition experiment,Trichosporon asahii Infected THP-1 Cells vs THP-1 Cells. Biological replicates: 3 infected THP-1 Cells, independently grown and harvested.One replicate per array.
2012-11-03 | E-GEOD-41983 | biostudies-arrayexpress
Project description:Citrate, a central component of cellular metabolism, is a widely used anti-coagulant due to its ability to chelate calcium. Adenosine triphosphate (ATP)-citrate lyase, which metabolizes citrate, has been shown to be essential for inflammation, but the ability of exogenous citrate to impact inflammatory signalling cascades remains largely unknown. We hypothesized that citrate would modulate inflammatory responses as both a cellular metabolite and calcium chelator, and tested this hypothesis by determining how clinically relevant levels of citrate modulate monocyte proinflammatory responses to lipopolysaccharide (LPS) in a human acute monocytic leukaemia cell line (THP-1). In normal medium (0•4 mM calcium), citrate inhibited LPS-induced tumour necrosis factor (TNF)-α and interleukin (IL)-8 transcripts, whereas in medium supplemented with calcium (1•4 mM), TNF-α and IL-8 levels increased and appeared independent of calcium chelation. Using an IL-8–luciferase plasmid construct, the same increased response was observed in the activation of the IL-8 promoter region, suggesting transcriptional regulation. Tricarballylic acid, an inhibitor of ATP-citrate lyase, blocked the ability of citrate to augment TNF-α, linking citrate's augmentation effect with its metabolism by ATP-citrate lyase. In the presence of citrate, increased histone acetylation was observed in the TNF-α and IL-8 promoter regions of THP-1 cells. We observed that citrate can both augment and inhibit proinflammatory cytokine production via modulation of inflammatory gene transactivation. These findings suggest that citrate anti-coagulation may alter immune function through complex interactions with the inflammatory response.
Research is published, core data not used but project description is relevant:
http://onlinelibrary.wiley.com/doi/10.1111/cei.12591/full
2015-06-11 | ST000202 | MetabolomicsWorkbench
Project description:Citrate, a central component of cellular metabolism, is a widely used anti-coagulant due to its ability to chelate calcium. Adenosine triphosphate (ATP)-citrate lyase, which metabolizes citrate, has been shown to be essential for inflammation, but the ability of exogenous citrate to impact inflammatory signalling cascades remains largely unknown. We hypothesized that citrate would modulate inflammatory responses as both a cellular metabolite and calcium chelator, and tested this hypothesis by determining how clinically relevant levels of citrate modulate monocyte proinflammatory responses to lipopolysaccharide (LPS) in a human acute monocytic leukaemia cell line (THP-1). In normal medium (0•4 mM calcium), citrate inhibited LPS-induced tumour necrosis factor (TNF)-α and interleukin (IL)-8 transcripts, whereas in medium supplemented with calcium (1•4 mM), TNF-α and IL-8 levels increased and appeared independent of calcium chelation. Using an IL-8–luciferase plasmid construct, the same increased response was observed in the activation of the IL-8 promoter region, suggesting transcriptional regulation. Tricarballylic acid, an inhibitor of ATP-citrate lyase, blocked the ability of citrate to augment TNF-α, linking citrate's augmentation effect with its metabolism by ATP-citrate lyase. In the presence of citrate, increased histone acetylation was observed in the TNF-α and IL-8 promoter regions of THP-1 cells. We observed that citrate can both augment and inhibit proinflammatory cytokine production via modulation of inflammatory gene transactivation. These findings suggest that citrate anti-coagulation may alter immune function through complex interactions with the inflammatory response.
Research is published, core data not used but project description is relevant:
http://onlinelibrary.wiley.com/doi/10.1111/cei.12591/full
2015-06-04 | ST000172 | MetabolomicsWorkbench
Project description:Examination of differentially expressed genes during monocyte to macrophage differentiation in THP-1 cells
2021-02-01 | GSE150571 | GEO
Project description:Macrophages play a key role in both innate and adaptive immunity, but our knowledge on the changes in transcription regulation that occurs during their differentiation from monocytes is still limited. In this study, we used a meta-analysis followed by a systems biology approach for the identification of differentially expressed genes between monocytes and macrophages and possible regulators of these changes in transcription. Based on the pattern of gene expression change, transcription regulator analysis predicted a decrease in Enhancer of Zeste homolog 2 (EZH2), a histone 3 lysine 27 methyl transferase, activity after differentiation of monocytes into macrophages. This inhibition was validated by a significant decrease in trimethylated H3K27 during differentiation of both human primary monocytes into macrophages and the THP-1 cell line into macrophage-like cells. Overexpressing EZH2 during differentiation of monocytes and THP-1 cells obstructs cellular adhesion, thus preventing the first step in differentiation. Another facet of macrophage differentiation is the cessation of proliferation, and inhibition of EZH2 by the small molecule inhibitor GSK126 in THP-1 cells indeed impedes proliferation. This study shows an important part for epigenetic changes during monocyte differentiation. It highlights the role of EZH2 activity behind the changes needed in adhesion and proliferation mechanisms for macrophage formation. THP-1s were differentiated into macrophage like cells by PMA stimulation.
2013-12-28 | E-GEOD-53691 | biostudies-arrayexpress
Project description:Background: Although genetic or epigenetic alterations have shown to affect the three-dimensional organization of genomes, the utility of chromatin conformation in the classification of human disease has never been addressed. Results: Here, we explore whether chromatin conformation can be used to classify human leukemia. We map the conformation of the HOXA gene cluster in a panel of cell lines with 5C chromosome conformation capture technology, and use the data to train and test a support vector machine classifier named 3D-SP. We show that 3D-SP is able to accurately distinguish leukemias expressing MLL-fusion proteins from those expressing only wild-type MLL, and that it can also classify leukemia subtypes according to MLL fusion partner, based solely on 5C data. Conclusions: Our study provides the first proof-of-principle demonstration that chromatin conformation contains the information value necessary for classification of leukemia subtypes. Examination of CTCF and RAD21 binding sites in THP-1 cell.
2014-02-27 | E-GEOD-55407 | biostudies-arrayexpress