Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of GSK3 inhibition on the transcriptional signature of human monocytes

ABSTRACT: We explored the molecular impact of blocking GSK3 on the gene expression profile in human monocytes. GSK3 inhibition by CHIR-99021 redirected monocytes towards acquiring an anti-inflammatory gene profile similar to M-CSF-primed monocyte-derived macrophages.

ORGANISM(S): Homo sapiens

PROVIDER: GSE256538 | GEO | 2025/04/16

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of GSK3 inhibition on the transcriptional signature of human GM-CSF-dependent monocyte-derived macrophages

Project description:The functional versatility of macrophages is intrincately tied to factors such as their ontogeny and the specific tissue and extracellular environment. Monocyte-derived macrophages are oppositely instructed by M-CSF or GM-CSF. GM-CSF drives monocyte-derived macrophages towards heightened pro-inflammatory activity and the acquisition of the lung alveolar macrophage phenotype and gene profile whereas M-CSF gives rise to anti-inflammatory, pro-resolving, and immunosuppressive monocyte-derived macrophages. We explored the molecular impact of blocking GSK3 on the gene expression profile in GM-CSF-primed human monocyte derived macrophages. GSK3 inhibition skewed the transcriptional profile of GM-MØ towards an anti-inflammatory phenotype.

2025-04-16 | GSE256208 | GEO

Effect of GSK3 inhibition on the transcriptional signature of human alveolar macrophages

Project description:The remarkable plasticity of macrophages is tied to extracelular cues and their subsequently signaling pathways. The transcriptional factor MAFB is critical to prompt the aquisition of an anti-inflammatory phenotype in macrophages. As MAFB activity and stability is highly regulated by GSK3, we explored the molecular impact of blocking GSK3 on the gene expression profile of human alveolar macrophages (AMØ), whose development and gene expression profile is GM-CSF-dependent. GSK3 inhibition skewed the transcriptional profile of AMØ towards an anti-inflammatory phenotype.

2025-04-16 | GSE262463 | GEO

Effect of GSK3 inhibition on the transcriptional signature of human monocytes

Project description:Effect of GSK3 inhibition on the transcriptional signature of human monocytes

| PRJNA1080033 | ENA

RNA-sequencing of human pluripotent stem-cell derived endothelial cells under control and Wnt-activating conditions

Project description:Endothelial cells (ECs) in the central nervous system (CNS) acquire specialized barrier properties in response to extrinsic signals, with Wnt/β-catenin signaling coordinating multiple aspects of endothelial barrier function. We used human pluripotent stem cell (hPSC)-derived endothelial progenitor cells to profile the EC response to Wnt activation using multiple strategies, including the small molecule GSK-3 inhibitor CHIR 99021, and the CNS-derived ligands Wnt7a and Wnt7b.

2021-11-10 | GSE173206 | GEO

GM-CSF induced gene-regulation in human monocytes

Project description:Human and murine studies showed that granulocyte macrophage colony-stimulating factor (GM-CSF) exerts beneficial effects in intestinal inflammation. To explore whether GM-CSF mediates its effects via monocytes, we analyzed effects of GM-CSF on monocytes in vitro and assessed the immunomodulatory potential of GM-CSF-activated monocytes (GMaM). We used microarray technology and functional assays to characterize GMaM in vitro and used a mouse model of colitis to study GMaM functions in vivo. Peripheral blood monocytes where cultured 16 h with media containing AB serum (control monocytes) or media containing 10 ng/mL GM-CSF and AB serum (GM-CSF activated monocytes). In three independent experiments, total RNA from GMaM and control monocytes was isolated and processed for microarray hybridization.

2014-11-27 | E-GEOD-63662 | biostudies-arrayexpress

The role of GSK3 on macrophage re-programming by high-dose methotrexate

Project description:Macrophage phenotypic and functional heterogeneity derives from tissue-specific transcriptional signatures shaped by the local microenvironment. M-CSF drives the generation of human monocyte-derived macrophages with a potent anti-inflammatory activity upon stimulation. One-carbon metabolism (OCM) is a complex network of biosynthetic pathways that includes de novo biosynthesis of purines and thymidylate, amino acid metabolism, and methylation reactions. Methotrexate (MTX) is an anti-folate drug used for Acute Lymphoblastic Leukemia treatment. We explored the molecular impact of blocking GSK3 a/b on the transcriptional effect of high-doses of MTX in M-CSF-primed human monocyte derived macrophages.

2023-10-01 | GSE185872 | GEO

Danger signal initiates differentiation of monocytes into osteopontin‑producing macrophages III

Project description:Purpose: We report the application of single-cell RNA sequencing for profiling the genexpression of different monocyte types in order to characterize monocytes that differentiate into macrophages under danger signal in comparison to conventional GM-CSF and M-CSF macrophages Methods: Monocytes freshly isolated from PBMCs were differentiated into GM-CSF, M-CSF, and danger-signal induced macrophages. Two million cells of each macrophage population were tagged accordingly with TotalSeq™‑B Hashtags. Single cell RNA sequencing was performed on all macrophage populations in order to characterize cells from each population. ScRNAseq analysis was performed with the R package Seurat on 16470 barcodes after filtering. Results: Cluster analysis reveals distinct separation of all three macrophage populations. Conclusion: The clear difference in overall gene expression profile suggests that macrophages exposed to danger signal differentiate into a novel macrophage type in contrast to conventional GM-CSF and M-CSF monocytes.

2022-01-11 | GSE180113 | GEO

Adipose stem cell-derived hepatocyte-like cells from obese patients reveal hepatic steatosis and mitochondrial oxidative dysfunction

Project description:Background & Aims: Obesity is the most important risk factor and a potential treatment target for fatty liver disease (FLD). The continuous adaptation or ‘remodelling’ of hepatic mitochondrial flexibility plays a key role in the pathogenesis of FLD. Human adipose stem cell (hASC)-derived hepatocyte-like cells (HLCs) offer attractive tools for the research and therapy of liver dysfunction. However, evidence showing the ‘remodelling’ of hepatic mitochondrial flexibility or differentiation capability of hASCs in obese patients is lacking. Methods: The differentiation capability and mitochondrial structure and function of hepatic cells were evaluated by measuring gene expression, de novo lipogenesis and mitochondrial respiration in HLCs derived from hASCs of obese patients and lean controls. The ability of the GSK3 inhibitor CHIR-99021 to modify the mitochondrial oxidative dysfunction was evaluated in the HLCs derived from the hASCs of obese patients. Results: hASCs from obese patients showed the potential to differentiate into HLCs. HLCs from the hASCs of obese patients exhibited the characteristics of hepatic steatosis, lower expression of the subunits of mitochondrial complex I and lower oxidative phosphorylation levels. CHIR-99021 promoted the expression of NDUFB8, NDUFB9, the subunits of mitochondrial complex I, and the basal oxygen consumption rate of the HLCs derived from the hASCs of obese patients by upregulating the expression of PGC-1α, the transcription factor involved in mitochondrial biogenesis and ‘remodelling’. Conclusions: The results demonstrate that obese patient ASC-derived HLCs had mitochondrial oxidative dysfunction, which may represent the consequence of hepatic steatosis.

2021-03-19 | GSE151760 | GEO

GM-CSF induced gene-regulation in human monocytes

2014-11-27 | GSE63662 | GEO

ChIP-seq of CSF-1R, H3K4me1, H3K4me3 in human primary unstimulated monocytes and monocytes differentiated 72h with CSF-1 (3 healthy donors buffy coat) and in monocytes from two CMML patients and one healthy donor, EGR1 ChIP-seq in unstimulated monocytes (3 healthy donors buffy coat)

Project description:Identification of nuclear CSF-1R, H3K4me1 and H3K4me3 localization on chromatin in human primary monocytes and modification of this localization during monocyte differentiation into macrophage induced by 100ng/mL CSF-1 during 6 hours (1 donor) or 72h (3 donors). Identification of EGR1 chromatin localization in human primary monocytes (3 donors) Comparison of nuclear CSF-1R chromatin localization in monocytes from 1 healthy donor and 2 chronic myelomonocytic leukemia patients.

2019-03-04 | E-MTAB-6305 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data