Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bulk RNA sequencing of chow diet mouse hepatocytes treated with iron chelator (DFO) and chow diet mouse hepatic stallete cells treated with iron

ABSTRACT: The goals of this study are to compare transcriptome profiling (RNA-seq) on iron of hepatocytes and stellate cells. Methods: mRNA profiles of wild-type (WT) NCD hepatocytes treated with or without DFO (100 uM) (n=6) and WT chow diet stellate cells treated with or without iron were generated by deep sequencing,

ORGANISM(S): Mus musculus

PROVIDER: GSE185694 | GEO | 2022/05/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Bulk RNA sequencing of chow diet mouse hepatocytes treated with iron chelator (DFO) and chow diet mouse hepatic stallete cells treated with iron

Project description:Bulk RNA sequencing of chow diet mouse hepatocytes treated with iron chelator (DFO) and chow diet mouse hepatic stallete cells treated with iron

| PRJNA770519 | ENA

Treatment of a human lymphoblastoid cell line with the iron chelator deferoxamine

Project description:We treated lymphoblast cells with the iron chelator deferoxamine (DFO) for 60 hours to determine if iron chelation would affect the levels of intron lariats.

2022-03-23 | GSE199077 | GEO

Gene expression of THP-1 macrophages co-cultured with F. nucleatum under iron-deficient and iron-overload conditions

Project description:Fusobacterium nucleatum (F. nucleatum) contributes to the development of colorectal cancer (CRC) by inducing chronic inflammation. We found that iron deposition in macrophages is associated with poor prognosis of CRC patients with high amount of F. nucleatum. To explore the impact of iron on macrophage properties in the presence of F. nucleatum, we conducted RNA sequencing of THP-1 macrophages pretreated with ferric anmonium citrate (FAC) or deferoxamine (DFO), followed by treatment with F. nucleatum. Several chemokine genes were differentially increased in FAC-treated cells when compared with DFO-treated cells, suggesting that iron is required for the efficient induction of tumor-promoting chemokines in macrophages upon F. nucleatum infection. Our results suggest a prognostic role for iron in F. nucleatum-positive CRC.

2022-08-21 | GSE192400 | GEO

Change expression of genes in iron chelation and deficient conditions

Project description:Firstly, cell senescence and anti-oxidant genes were down-regulated by iron deficient mice and iron-specific chelator deferoxamine (DFO) using a DNA microarray. Our data suggested that down-regulation of anti-oxidant genes and cell senescence gene induced oxidative stress in iron-deficient and -specific chelated condition.

2018-01-26 | GSE109656 | GEO

Transcriptomics analysis of iron chelator deferoxamine treated human tumor colonoids.

Project description:To investigate the detailed molecular mechanisms for the regulatory role of iron in colorectal cancer, RNA-seq analysis was performed on RNA isolated from untreated control and deferoxamine treated human tumor colonoids.

2023-08-01 | GSE185738 | GEO

Single cell RNA-seq of mouse HSC treated with iron chelator deferoxamine (DFO)

Project description:We characterized longer-term effects of iron homeostasis activation on hematopoietic stem cells by characterizing transcriptomic chagnes at the singe cell level 48hrs after iron chelatior treatement (vehicle treatemnt as controls).

2024-05-02 | GSE157821 | GEO

RNAseq Iron-Treated iPSC-derived Microglia

Project description:Iron accumulation in microglia has been observed in AlzheimerÃ¢Â€Â™s disease and other neurodegenerative disorders and is thought to contribute to disease progression through various mechanisms including neuroinflammation. To study the interaction between iron accumulation and inflammation, we treated human induced pluripotent stem cell-derived microglia (iPSC-MG) with an increasing concentration of iron, in combination with inflammatory stimuli such as interferon gamma and amyloid ÃŽÂ², and performed RNA sequencing.

| EGAS00001006112 | EGA

Intracellular labile iron is a key regulator of hepcidin expression and iron metabolism

Project description:Liver iron overload can induce hepatic expression of hepcidin and regulates iron metabolism. However, the mechanism of iron regulating iron metabolism remains known. Intracellular labile iron represents the nonferritin-bound, redox-active iron which is transitory and serves as a crossroad of cell iron metabolism. The role of intracellular labile iron played in iron metabolism has largely been elucidated. Here we show that intracellular labile iron of hepatocytes has dual function in iron metabolism. It can induce hepatocytes expressing hepcidin via ER stress induced transcription factors on the one hand, on the other hand stimulate BMP2 and BMP6 expression of liver sinusoidal endothelial cells (LSECs) though TNFα secreted by hepatocytes to further regulate iron metabolism. Blockade of TNFα could dysregulate the iron metabolism during iron overload. Our findings reveal the important role of intracellular labile iron in iron metabolism and represent a novel way to modulate iron metabolism during iron overload.

2023-05-03 | GSE186655 | GEO

Iron Chelators Treatment on DMS-53 Human Lung Cancer Cell

Project description:The molecular role of iron in gene expression remains poorly characterized. Moreover, the alterations in global gene expression after iron chelation remains unclear and are important to assess for understanding the molecular pathology of iron-depletion and the biological effects of iron chelators. We assessed the effect on whole genome gene expression of two iron chelators (desferrioxamine and Dp44mT). These studies are important for understanding the molecular and cellular effects of iron-depletion. The DMS-53 cells were incubated with either control medium or this medium containing DFO (250 µM) or Dp44mT (25 µM) for 24 h at 37oC. These concentrations were used since our previous studies demonstrated that under these conditions these chelators lead to up-regulation of iron-responsive genes such as the TfR1 after this incubation time. Moreover, the higher concentration of DFO was implemented due to its limited ability to permeate cell membranes. Total RNA was isolated from cells in 1 mL of TRIzol® reagent (Invitrogen). Samples were then prepared and hybridized to the Human Genome U133 Plus 2.0 430 2.0. The human GeneChip® U133 Plus 2.0 consists of greater than 47,000 transcripts and variants from over 38,500 well characterized human genes. On completion of hybridization and washing, microarray chips were scanned with the Affymetrix GeneChip® Scanner 3000 (Affymetrix).

2011-12-31 | E-GEOD-26920 | biostudies-arrayexpress

Single cell RNA-seq of liver cells from B6J mice fed a chow or a high-fat-and-high-sucrose diet

Project description:Cannabinoid receptor-1 (CB-1) blockage in brain is responsible for weight loss, many of the metabolic benefits associated with CB-1 blockade have been attributed to inhibition of CB-1 signaling in the periphery. We produced mice that lacked CB-1 receptors in hepatocytes or stellate cells to determine if CB-1 signaling contributes to the development of NAFLD or liver fibrosis. Deletion of CB-1 receptors in hepatocytes did not alter the development of NAFLD in mice fed a high sucrose high fat diet (HSD) or high fat diet (HFD). Similarly, deletion of CB-1 deletion specifically in stellate cells also did not prevent the development of NAFLD in mice fed the HFD nor did it protect mice for carbon tetrachloride-induced fibrosis. To determine if a small population of cells in liver express CB-1 at high levels either before and/or after HSD feeding, here we performed single cell RNA-sequencing of livers from wild-type mice fed chow or a HSD for 17 weeks and analyzed CB-1 expression. Single-cell sequencing of hepatocytes and stellate cells reveals low Cnr1 expression in livers of mice fed a chow or HSD. Combined, these studies do not support a direct role for hepatocyte or stellate cell CB-1 signaling in the development of NAFLD or liver fibrosis.

2021-09-01 | GSE182365 | GEO

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