We are analyzing https://link.springer.com/article/10.1007/s11033-013-2792-z.

Title:
Protective effect of mitochondrial ferritin on cytosolic iron dysregulation induced by doxorubicin in HeLa cells | Molecular Biology Reports
Description:
Doxorubicin (DOX) is an anticancer drug with cardiotoxic side effects mostly caused by iron homeostasis dysregulation. Mitochondria are involved in iron trafficking and mitochondrial ferritin (FtMt) was shown to provide protection against cellular iron imbalance. Therefore, we hypothesized that FtMt overexpression could limit DOX effects on iron homeostasis. Heart’s homogenates of DOX-treated C57BL/6 mice were analyzed for cytosolic and mitochondrial iron-related proteins’ expression and activity, revealing high cytosolic ferritin and ferritin-bound iron, low transferrin-receptor 1 and a strong hepcidin upregulation. Mitochondrial iron-related proteins (aconitase, succinate-dehydrogenase, frataxin) seemed, however, unaffected, although a partial inactivation of superoxide dismutase 2 was detected. Importantly, the ectopic expression of FtMt in human HeLa cells partially reverted DOX-induced iron imbalance. Our results, while confirming DOX effects on iron homeostasis, demonstrate that DOX affects more cytosolic than mitochondrial iron metabolism both in murine hearts and human HeLa cells and that FtMt overexpression is able to prevent most of these effects in HeLa cells.
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article, iron, pubmed, google, scholar, cas, mitochondrial, ferritin, cells, doxorubicin, hela, access, cocco, derosas, biasiotto, metabolism, cardiotoxicity, mol, privacy, cookies, content, molecular, cytosolic, zanella, effects, expression, biol, levi, supplementary, material, pdf, information, publish, search, protective, september, emiliano, porrini, dox, homeostasis, ftmt, mice, proteins, hepcidin, frataxin, human, open, cardiac, toxicity, blood,

Topics {✒️}

month download article/chapter federica maccarinelli & isabella zanella mitochondrial iron-related proteins dox-treated c57bl/6 mice cellular iron imbalance iron regulatory proteins mitochondrial iron overload iron homeostasis dysregulation ubiquitin-proteasome pathway human mitochondrial ferritin iron metabolism induced human hela cells full article pdf cardiac iron metabolism privacy choices/manage cookies mitochondrial iron metabolism anthracycline-induced cardiotoxicity mitochondrial iron trafficking ferritin-bound iron free cellular iron mitochondrial ferritin expression mitochondrial abcb7 transporter iron-deficient phenotype iron-mediated toxicity mammalian iron metabolism iron-dependent degradation strong hepcidin upregulation adriamycin-cardiolipin complex protective effect hela cells published article cocco oxidative stress supplying mt53 cells doxorubicin-treated mice iron homeostasis iron-dependent regulation european economic area low transferrin-receptor 1 st clair dk adult mouse tissues reactive oxygen species limit dox effects confirming dox effects conditions privacy policy check access instant access irp1-independent alterations isabella zanella cardiotoxic side effects accepting optional cookies

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         headline:Protective effect of mitochondrial ferritin on cytosolic iron dysregulation induced by doxorubicin in HeLa cells
         description:Doxorubicin (DOX) is an anticancer drug with cardiotoxic side effects mostly caused by iron homeostasis dysregulation. Mitochondria are involved in iron trafficking and mitochondrial ferritin (FtMt) was shown to provide protection against cellular iron imbalance. Therefore, we hypothesized that FtMt overexpression could limit DOX effects on iron homeostasis. Heart’s homogenates of DOX-treated C57BL/6 mice were analyzed for cytosolic and mitochondrial iron-related proteins’ expression and activity, revealing high cytosolic ferritin and ferritin-bound iron, low transferrin-receptor 1 and a strong hepcidin upregulation. Mitochondrial iron-related proteins (aconitase, succinate-dehydrogenase, frataxin) seemed, however, unaffected, although a partial inactivation of superoxide dismutase 2 was detected. Importantly, the ectopic expression of FtMt in human HeLa cells partially reverted DOX-induced iron imbalance. Our results, while confirming DOX effects on iron homeostasis, demonstrate that DOX affects more cytosolic than mitochondrial iron metabolism both in murine hearts and human HeLa cells and that FtMt overexpression is able to prevent most of these effects in HeLa cells.
         datePublished:2013-09-25T00:00:00Z
         dateModified:2013-09-25T00:00:00Z
         pageStart:6757
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            Cardiotoxicity
            Iron
            Mitochondrial ferritin
            Hepcidin
            Animal Biochemistry
            Animal Anatomy / Morphology / Histology
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      headline:Protective effect of mitochondrial ferritin on cytosolic iron dysregulation induced by doxorubicin in HeLa cells
      description:Doxorubicin (DOX) is an anticancer drug with cardiotoxic side effects mostly caused by iron homeostasis dysregulation. Mitochondria are involved in iron trafficking and mitochondrial ferritin (FtMt) was shown to provide protection against cellular iron imbalance. Therefore, we hypothesized that FtMt overexpression could limit DOX effects on iron homeostasis. Heart’s homogenates of DOX-treated C57BL/6 mice were analyzed for cytosolic and mitochondrial iron-related proteins’ expression and activity, revealing high cytosolic ferritin and ferritin-bound iron, low transferrin-receptor 1 and a strong hepcidin upregulation. Mitochondrial iron-related proteins (aconitase, succinate-dehydrogenase, frataxin) seemed, however, unaffected, although a partial inactivation of superoxide dismutase 2 was detected. Importantly, the ectopic expression of FtMt in human HeLa cells partially reverted DOX-induced iron imbalance. Our results, while confirming DOX effects on iron homeostasis, demonstrate that DOX affects more cytosolic than mitochondrial iron metabolism both in murine hearts and human HeLa cells and that FtMt overexpression is able to prevent most of these effects in HeLa cells.
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      dateModified:2013-09-25T00:00:00Z
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         Cardiotoxicity
         Iron
         Mitochondrial ferritin
         Hepcidin
         Animal Biochemistry
         Animal Anatomy / Morphology / Histology
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