We are analyzing https://link.springer.com/article/10.1007/s00109-006-0068-y.

Title:
IRP1-independent alterations of cardiac iron metabolism in doxorubicin-treated mice | Journal of Molecular Medicine
Description:
Iron aggravates the cardiotoxicity of doxorubicin (DOX), a widely used anticancer anthracycline. The amount of iron in the cell is regulated by the iron regulatory proteins (IRPs)-1 and -2 that control the posttranscriptional expression of key iron metabolism genes. In vitro and cell culture studies revealed the ability of DOX to modulate the activity of both IRPs. However, conflicting data were obtained from different cell types and experimental conditions. To investigate the connection between acute DOX cardiotoxicity and the IRPs in a mammalian organism, we analyzed IRP activity and the expression of IRP target genes in the heart of mice subjected to DOX treatment. DOX exposure elicits a differential modulation of the two IRPs with reduced IRP2 activity and unchanged IRP1 activity. IRP2 downmodulation is associated with the upregulation of the ferritin L and H genes and decreased expression of the transferrin receptor 1 (TfR1). To directly test the role of IRP1 in DOX cardiotoxicity, the DOX response was analyzed in mice lacking IRP1. DOX-mediated IRP2 downmodulation and regulation of ferritin and TfR1 expression is identical in Irp1 −/− mice compared to wild type, as is the degree of oxidative damage of the heart assessed by thioredoxin and thiobarbituric acid reactive substance levels and by brain natriuretic peptide mRNA expression. These data demonstrate that the alterations of cardiac iron homeostasis related to acute anthracycline cardiotoxicity occur independently of IRP1. The observed IRP2 downmodulation could serve as a means to counteract DOX cardiotoxicity by reducing the “free” cellular iron pool.
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Keywords {🔍}

article, pubmed, google, scholar, cas, iron, irp, cardiotoxicity, regulatory, mice, cairo, expression, ferritin, protein, doxorubicin, dox, activity, molecular, metabolism, galy, hentze, cell, heart, cardiac, genes, role, regulation, privacy, cookies, content, data, journal, anthracycline, proteins, minotti, anthracyclines, cells, blood, biol, chem, analysis, publish, search, alterations, corna, irps, related, access, doxorubicininduced, med,

Topics {✒️}

iron-regulatory protein-rna-binding activity month download article/chapter left-ventricular systolic dysfunction oxidant-induced iron signaling end-stage heart failure p38-mapk/nf-κb unexpected anthracycline-mediated alterations iron regulatory proteins distinct metabolic pathways doxorubicin-resistant cancer cells full article pdf iron-regulatory protein 2 dox-mediated irp2 downmodulation doxorubicin-induced cardiotoxicity iron-mediated toxicity european economic area iron-dependent stability doxorubicin-induced cardiomyopathy iron metabolism induced cardiac iron metabolism article corna privacy choices/manage cookies related subjects molecular medicine aims thiobarbituric acid reaction doxorubicin-treated mice irp1-independent alterations �free” iron pool heavy subunit sequences iron-mediated cardiotoxicity nf-kappab activation reactive oxygen species tumor necrosis factor rt-pcr analysis reduced irp2 activity gaetano cairo observed irp2 downmodulation acute dox cardiotoxicity ferritin gene expression superoxide dismutase activity heart cell mitochondria transformed endothelial cells doxorubicin-mediated apoptosis rat heart cells unchanged irp1 activity secondary alcohol metabolite increased mitochondrial efficiency maria paola santini article journal doxorubicin-induced

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         description:Iron aggravates the cardiotoxicity of doxorubicin (DOX), a widely used anticancer anthracycline. The amount of iron in the cell is regulated by the iron regulatory proteins (IRPs)-1 and -2 that control the posttranscriptional expression of key iron metabolism genes. In vitro and cell culture studies revealed the ability of DOX to modulate the activity of both IRPs. However, conflicting data were obtained from different cell types and experimental conditions. To investigate the connection between acute DOX cardiotoxicity and the IRPs in a mammalian organism, we analyzed IRP activity and the expression of IRP target genes in the heart of mice subjected to DOX treatment. DOX exposure elicits a differential modulation of the two IRPs with reduced IRP2 activity and unchanged IRP1 activity. IRP2 downmodulation is associated with the upregulation of the ferritin L and H genes and decreased expression of the transferrin receptor 1 (TfR1). To directly test the role of IRP1 in DOX cardiotoxicity, the DOX response was analyzed in mice lacking IRP1. DOX-mediated IRP2 downmodulation and regulation of ferritin and TfR1 expression is identical in Irp1 −/− mice compared to wild type, as is the degree of oxidative damage of the heart assessed by thioredoxin and thiobarbituric acid reactive substance levels and by brain natriuretic peptide mRNA expression. These data demonstrate that the alterations of cardiac iron homeostasis related to acute anthracycline cardiotoxicity occur independently of IRP1. The observed IRP2 downmodulation could serve as a means to counteract DOX cardiotoxicity by reducing the “free” cellular iron pool.
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