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.
Project description:We found that iron chelation restored functional defects in aged HSC, including engraftment potential and platelet bias. To gain molecular insights into iron-dependent mechanism for sustaining HSC identity during aging, we performed Cellular Indexing of Transcriptomes and Epitopes by Sequencing (CITE-seq) with lineage (Lin)− Sca-1+ cKit+ (LSK) cells isolated from aged mice after long-term regimens with iron chelator Deferoxamine or vehicle control.
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.
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.
Project description:TIGR4 and R6 bacterial strains of Streptococcus pneumoniae treated and not treated with the iron chelator deferoxamine mesylate (DFO)
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.
Project description:Adipocyte differentiation has been shown to require iron, but the underlying mechanism remains elusive. Ferrous iron ion is known to function as a co-factor for alpha-ketoglutarate-dependent dioxygenases, including demethylases for histones, DNA, and RNA. Previously we reported several alpha-ketoglutarate-dependent histone demethylases as critical epigenetic regulators during adipogenesis. These lines of evidence led us to hypothesize that iron orchestrates epigenetic/epitranscriptional regulations during adipogenesis by controlling demethylation activities. In this study, we conducted genome-wide analysis on methylation landscapes of histones, DNA, and RNA in differentiation of 3T3-L1 pre-adipocytes. Using the iron chelator deferoxamine, we demonstrate here how dynamically methylation levels of histones, DNA, and RNA are regulated by iron during adipogenesis.
Project description:Adipocyte differentiation has been shown to require iron, but the underlying mechanism remains elusive. Ferrous iron ion is known to function as a co-factor for alpha-ketoglutarate-dependent dioxygenases, including demethylases for histones, DNA, and RNA. Previously we reported several alpha-ketoglutarate-dependent histone demethylases as critical epigenetic regulators during adipogenesis. These lines of evidence led us to hypothesize that iron orchestrates epigenetic/epitranscriptional regulations during adipogenesis by controlling demethylation activities. In this study, we conducted genome-wide analysis on methylation landscapes of histones, DNA, and RNA in differentiation of 3T3-L1 pre-adipocytes. Using the iron chelator deferoxamine, we demonstrate here how dynamically methylation levels of histones, DNA, and RNA are regulated by iron during adipogenesis.
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. 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).