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Iron excess limits HHIPL2 gene expression and decreases osteoblastic activity in human MG-63 cells

ABSTRACT: Our transcriptomic data shows that iron impact on human osteoblastic MG-63 cells by decreasing HHIPL-2 gene expression (2 fold ratio). This impact is corrected in presence of deferoxamine. Additional biological experiments in the manuscript suggest that the iron related modulation of HHIPL-2 gene expression could take place in the decrease of osteoblastic markers in the MG-63 cell line. Such mechanisms could participate to the development of osteoporosis in iron overloaded patients. One-condition experiment, iron exposure using ferric ammonium citrate (FAC) at two concentrations (5 and 20M-BM-5M) was compared to basal condition. Additional conditions include: deferoxamine (DFO) (iron chelator) 20M-BM-5M alone or in addition to FAC 20M-BM-5M. For each condition five biological replicates were performed (independent experiments).

ORGANISM(S): Homo sapiens

SUBMITTER: DOYARD Mathilde

PROVIDER: E-GEOD-30774 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Iron excess limits HHIPL2 gene expression and decreases osteoblastic activity in human MG-63 cells

Project description:Our transcriptomic data shows that iron impact on human osteoblastic MG-63 cells by decreasing HHIPL-2 gene expression (2 fold ratio). This impact is corrected in presence of deferoxamine. Additional biological experiments in the manuscript suggest that the iron related modulation of HHIPL-2 gene expression could take place in the decrease of osteoblastic markers in the MG-63 cell line. Such mechanisms could participate to the development of osteoporosis in iron overloaded patients.

2012-09-01 | GSE30774 | GEO

Iron regulation in Vibrio vulnificus CMCP6

Project description:Vibrio vulnificus multiply rapidly in host tissues under iron overloaded conditions. To understand the effects of iron in the physiology of this pathogen we performed a genome-wide transcriptional analysis of this bacterium growing under three different iron concentrations. V.vulnificus CMCP6 cells were grown under three different iron concentrations (TSBS + EDDA 50uM, TSBS and TSBS + FAC 250 ug/ml) and samples taken at log phase. Keywords: Response to the iron concentration of the media Strains were grown to an OD600nm of 0.6 to 0.8 in TSBS, TSBS with the addition of 250 Î¼g/ml FAC or TSBS with the addition of 50 Î¼M EDDA. Three independent cultures of the V. vulnificus cells grown in each media, were combined and treated as a single sample for the RNA extraction to minimize culture variation. Two samples per condition were used for the microarray analysis. Cells were centrifuged and the pellets resuspended in RNAWiz reagent (AmbionÂ®, Austin, TX). Total RNA was extracted from each strain according to the manufacturerâ??s instructions

2010-05-25 | E-GEOD-10633 | biostudies-arrayexpress

Iron regulation in Vibrio vulnificus CMCP6

2008-08-07 | GSE10633 | 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

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.

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Gene expression profiles of B cells under various conditions

Project description:To validate the functions that iron might play in B cell proliferation and function we used deferoxamine (DFO, a widely used iron chelator) to create an iron-deficient environment for cell culture in vitro.

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Streptococcus pneumoniae. Two-color microarray bases Gene Expression Analysis v.6.5

Project description:TIGR4 and R6 bacterial strains of Streptococcus pneumoniae treated and not treated with the iron chelator deferoxamine mesylate (DFO)

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Transcription profiling of human CaCo-2 cells following various iron treatments

Project description:We investigated transcriptional response of CaCo-2 cells to iron treatments, we studied hemin effect by adding hemin to DMEM-FBS medium and iron deficiency effects in using an iron free medium compared to the same supplemented with FAC (ferric ammonium citrate). Experiment Overall Design: Biological replicates were used (3 samples) of each iron treatments (SF-FAC, SF-0, DMEM-FBS, DMEM-Hemin). Each sample was labelled with cy5 and a pool of each sample was constituted and labelled with cy3.

2008-01-19 | E-GEOD-3573 | biostudies-arrayexpress

Iron loading induces cholesterol synthesis and sensitizes endothelial cells to TNFα-mediated apoptosis

Project description:In plasma, iron is normally bound to transferrin, but in conditions of iron overload when the iron-binding capacity of transferrin is exceeded, non-transferrin-bound iron (NTBI) appears in plasma. NTBI is taken up by hepatocytes and other parenchymal cells via NTBI transporters and can cause cellular damage by promoting the generation of reactive oxygen species. However, how NTBI affects endothelial cells, the most proximal cell type exposed to circulating NTBI, has not been explored. We modeled in vitro the effects of systemic iron overload on endothelial cells by treating primary human umbilical vein endothelial cells (HUVECs) with NTBI (ferric ammonium citrate, FAC). Using an unbiased approach, we showed by RNA-Seq that iron loading alters lipid homeostasis in HUVECs by inducing SREBP2-mediated cholesterol biosynthesis. We also determined that FAC increased the susceptibility of HUVECs to apoptosis induced by TNFα. Moreover, we showed that cholesterol biosynthesis contributes to iron-potentiated apoptosis. Treating HUVECs with a cholesterol chelator hydroxypropyl-β-cyclodextrin demonstrated that depletion of cholesterol was sufficient to rescue HUVECs from TNFa-induced apoptosis, even in the presence of FAC. Finally, we showed that FAC or cholesterol treatment modulated the TNFα pathway by inducing novel proteolytic processing of TNFR1 to a short isoform that localizes to lipid rafts. Our study raises the possibility that iron-mediated toxicity in human iron overload disorders is at least in part dependent on alterations in cholesterol metabolism in endothelial cells, increasing their susceptibility to apoptosis.

2021-09-01 | GSE168534 | GEO

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