Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Microarray expression in whole brain of Hfe-/-xTfr2mut (double mut) vs wildtype (wt) AKR mice

ABSTRACT: Transcriptome changes were studied in the brain of 13 week male AKR mice with disruption of two iron regulatory genes, hemochromatosis Hfe and transferrin receptor 2 (Tfr2) compared to age and gender matched wildtype controls. The characterization of these mice is developed by Delima et al. 2012 (Delima, R. D., A. C. G. Chua, J. E. E. Tirnitz-Parker, E. K. Gan, K. D. Croft, R. M. Graham, J. K. Olynyk and D. Trinder (2012). Disruption of hemochromatosis protein and transferrin receptor 2 causes iron-induced liver injury in mice. Hepatology 56(2): 585-593.)

ORGANISM(S): Mus musculus

PROVIDER: GSE70431 | GEO | 2017/02/09

SECONDARY ACCESSION(S): PRJNA288676

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data from Hfe-deficient liver and duodenum in mouse strains with differing susceptibilities to iron loading

Project description:Hfe disruption in the mouse leads to experimental hemochromatosis by a mechanism which remains elusive. Evidence for at least five modifier genes has been obtained. These account for the higher iron load of Hfe-deficient D2 mice compared to B6 mice. Gene expression profling was used to clarify the mechanism of Hfe action and to identify potential modifier genes. Keywords: response to genetic modification

2008-03-22 | GSE7357 | GEO

Transcription profiling of Hfe-deficient liver and duodenum in mouse strains with differing susceptibilities to iron loading

2008-04-04 | E-GEOD-7357 | biostudies-arrayexpress

Effects of Hfe-/- and dietary iron overload on gene expression in the liver and duodenum of mice

Project description:Iron is an essential trace element whose absorption is usually tightly regulated in the duodenum. HFE-related hereditary hemochromatosis (HH) is characterized by abnormally low expression of the iron-regulatory hormone, hepcidin, which results in increased iron absorption. The liver is crucial for iron homeostasis as it is the main production site of hepcidin. The aim of this study was to explore and compare the genome-wide transcriptome response to Hfe deficiency and dietary iron overload in murine liver and duodenum.

2009-09-05 | GSE17969 | GEO

Transcription profiling of mouse lipopolysaccharide-induced inflammation in HFE-deficient and wild types

Project description:Inflammation influences iron balance in the whole organism. A common clinical manifestation of these changes is the anemia of chronic disease (ACD; also called anemia of inflammation). Inflammation reduces duodenal iron absorption and increases macrophage iron storage, resulting in low serum iron concentrations (hyposideremia). Despite the protection hyposideremia provides against proliferating microorganisms, this iron withholding reduces the iron available to developing red blood cells and eventually contributes to the development of anemia. Hepcidin antimicrobial peptide (Hamp) is a hepatic defensin-like peptide hormone that inhibits duodenal iron absorption and macrophage iron release. Hamp has antimicrobial activity and is part of the type II acute phase response. It is also thought to play a critical regulatory role in the sequestration of iron in the context of ACD. We report that mice with deficiencies in the hemochromatosis gene product, Hfe, mount a general inflammatory response, but lack appropriate Hamp expression and fail to develop hyposideremia. These data suggest a previously unidentified role for Hfe in innate immunity and ACD.

2004-03-15 | E-MEXP-95 | biostudies-arrayexpress

Transcription profiling of liver from wild type and Hfe-/- mice with hereditary hemochromatosis subjected to dietary iron overload and treatment with nifedipine to reverse iron overload

Project description:Hereditary hemochromatosis and transfusional iron overload are frequent clinical conditions associated with progressive iron accumulation in parenchymal tissues leading to eventual organ failure. We have discovered a novel mechanism to reverse iron overload by pharmacological modulation of the divalent metal transporter-1 (DMT-1). DMT-1 mediates intracellular iron transport during the transferrin cycle and apical iron absorption in the duodenum. Additional functions in iron handling in the kidney and liver are less well understood. We show that the L- type calcium-channel blocker nifedipine increases DMT-1 mediated cellular iron transport 10-to 100-fold at concentrations between 1-100 uM. Mechanistically, nifedipine causes this effect by prolongation of the activity of DMT-1 to transport iron. We show that nifedipine mobilizes iron from the liver of mice with primary and secondary iron overload, and enhances urinary iron excretion. Modulation of DMT-1 function by L-type calcium-channel blockers emerges a novel pharmacological concept to treat iron overload disorders.<br> <br> In this experiment mice were subjected to dietary iron overload before being treated with nifedipine at 5 ug/g bodyweight, or mock treated with the same volume of solvent.

2007-03-01 | E-MEXP-982 | biostudies-arrayexpress

Disrupted iron homeostasis causes dopaminergic neurodegeneration in mice

Project description:Disruption of local iron homeostasis is a common feature of neurodegenerative diseases. We focused on dopaminergic neurons, asking how iron transport proteins modulate iron homeostasis in vivo. Inactivation of the transmembrane iron exporter ferroportin had no apparent consequences. However, loss of the transferrin receptor 1, involved in iron uptake, caused profound, age-progressive neurodegeneration with features similar to Parkinson’s disease. There was gradual loss of dopaminergic projections in the striatum with subsequent death of dopaminergic neurons in the substantia nigra. After depletion of 30% of the neurons the mice developed neurobehavioral parkinsonism, with evidence of mitochondrial dysfunction and impaired mitochondrial autophagy. Molecular analysis revealed strong signatures indicative of attempted axonal regeneration, a metabolic switch to glycolysis and the unfolded protein response. We speculate that cellular iron deficiency may contribute to neurodegeneration in human patients Using Ribotag technology, from mouse ventral midbrain lysates, we isolated actively translated mRNA species from control and Transferrin receptor 1-null dopaminergic neurons. Two mouse ages were used 3 wks (early neurodegeration) 10 wks (late neurodegeneration)

2015-03-11 | E-GEOD-66730 | biostudies-arrayexpress

RNA-seq analysis of sorted duodenum epithelial cells and duodenum lamia propria macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

Project description:Iron is an essential cellular and important for many physiological functions including erythropoiesis and host defense. It is taken up from the diet in the duodenum, the first part of the small intestine by enterocytes and loaded onto transferrin, the main iron transport molecules in the circulation. Macrophages are ancient sentinel cells that are implicated in all steps of systemic iron metabolism except duodenal iron import. By assessing mice that harbor a macrophage-specific deletion of the tuberous sclerosis complex 2 (Tsc2), a negative regulator of mTORC1, we found that these mice possessed various defects in iron metabolism including defective steady state erythropoiesis and a highly reduced saturation of transferrin with iron. This iron-deficiency phenotype was caused by a block of iron import from the duodenal epithelial cells into the circulation. Activation of mTORC1 in villous duodenal CD68+ macrophages induced expression of serine proteases and promoted local degradation of the major iron transport molecule transferrin, whereas depletion of macrophages in mice increased transferrin levels in the duodenal villi. Inhibition of serine protease activity restored transferrin levels in the Tsc2-deficient mice. Physiologically, transferrin levels were regulated in the villi during Citrobacter rodentium infection in mice. These data show that transferrin is controlled locally in the duodenum and establish macrophages as regulators of duodenal iron uptake.

2023-06-08 | GSE196815 | GEO

scRNA-seq analysis of duodenum CD68+ macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

Project description:Iron is an essential cellular trace element and important for many physiological functions including erythropoiesis and host defense. It is taken up from the diet in the duodenum, the first part of the small intestine by enterocytes and loaded onto transferrin, the main iron transport molecules in the circulation. Macrophages are ancient sentinel cells that are implicated in all steps of systemic iron metabolism except duodenal iron import. By assessing mice that harbor a macrophage-specific deletion of the tuberous sclerosis complex 2 (Tsc2), a negative regulator of mTORC1, we found that these mice possessed various defects in iron metabolism including defective steady state erythropoiesis and a highly reduced saturation of transferrin with iron. This iron-deficiency phenotype was caused by a block of iron import from the duodenal epithelial cells into the circulation. Activation of mTORC1 in villous duodenal CD68+ macrophages induced expression of serine proteases and promoted local degradation of the major iron transport molecule transferrin, whereas depletion of macrophages in mice increased transferrin levels in the duodenal villi. Inhibition of serine protease activity restored transferrin levels in the Tsc2-deficient mice. Physiologically, transferrin levels were regulated in the villi during Citrobacter rodentium infection in mice. These data show that transferrin is controlled locally in the duodenum and establish macrophages as regulators of duodenal iron uptake.

2023-06-08 | GSE197175 | GEO

Effects of RGMc on BMP2 and BMP6-mediated Gene Expression in Hep3B Liver Cells

Project description:Mutations in repulsive guidance molecule c (RGMc) / hemojuvelin (HJV) cause juvenile hemochromatosis, an aggravated iron overload disorder that presents early in life. Patients with juvenile hemochromatosis, and RGMc knockout mice, have diminished expression of the key iron-regulatory peptide, hepcidin. This suggests that RGMc plays a critical role in the regulation of iron homeostasis; however the mechanisms of RGMc actions are unknown. Recent studies have shown that RGMc directly binds to the growth factors, bone morphogenetic protein 2 and 6 (BMP2 and BMP6), and it is possible that this interaction regulates aspects of iron metabolism. We used microarrays to examine the effects of RGMc on BMP2- and BMP6-mediated gene expression.

2010-06-15 | GSE20671 | GEO

Transcription profiling of mouse duodenum and liver with primary (Hfe ?/? and C282Y homozygous mice) and secondary iron overload vs 129S6/SvEvTac wild type controls

Project description:We determined duodenal and liver gene response patterns in mice with primary (Hfe ?/? and C282Y homozygous mice) and secondary iron overload versus 129S6/SvEvTac wild type controls.

2013-01-30 | E-MEXP-5 | 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