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Keywords {🔍}

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Topics {✒️}

construct named pbsk + 5-b-n-3 article download pdf b-type natriuretic peptide proto script m-mulv semi-thin slices showed dario finazzi iron-dependent oxidative damage hybrid pgk-em7 promoter common fwd-primer upstream bio-rad protein assay anthracycline-dependent oxidative injury rt-pcr analyses showed mitochondrial ferritin-deficient mice doxorubicin-induced cardiomyopathy original author low-risk myelodysplastic syndromes semi-thin sections kaplan-meier plot ten ftmt-deficient mice irp1-independent alterations end-stage heart failure author information authors mock-treated ftmt−/− mice common fwd primer privacy choices/manage cookies full access sideroblastic erythroid progenitors β-gal transcript encoded mitochondrial ferritin affects performed biochemical analyses doxorubicin-treated ftmt−/− mice reduced iron availability mitochondrial iron accumulation real-time pcr severe mitochondrial damage mitochondrial ferritin protects cardiac morphological alterations iron overload human mitochondrial ferritin mitochondrial iron deposits b-gal activity mouse mitochondrial ferritin produced siderocytes/sideroblasts similar control wild-type mice mitochondrial ferritin expression intracellular reactive iron exercise protects increases oxidative damage full mouse gene iron metabolism induced

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         headline:Mice lacking mitochondrial ferritin are more sensitive to doxorubicin-mediated cardiotoxicity
         description:Mitochondrial ferritin is a functional ferritin that localizes in the mitochondria. It is expressed in the testis, heart, brain, and cells with active respiratory activity. Its overexpression in cultured cells protected against oxidative damage and reduced cytosolic iron availability. However, no overt phenotype was described in mice with inactivation of the FtMt gene. Here, we used the doxorubicin model of cardiac injury in a novel strain of FtMt-null mice to investigate the antioxidant role of FtMt. These mice did not show any evident phenotype, but after acute treatment to doxorubicin, they showed enhanced mortality and altered heart morphology with fibril disorganization and severe mitochondrial damage. Signs of mitochondrial damage were present also in mock-treated FtMt−/− mice. The hearts of saline- and doxorubicin-treated FtMt−/− mice had higher thiobarbituric acid reactive substance levels, heme oxygenase 1 expression, and protein oxidation, but did not differ from FtMt+/+ in the cardiac damage marker B-type natriuretic peptide (BNP), ATP levels, and apoptosis. However, the autophagy marker LC3 was activated. The results show that the absence of FtMt, which is highly expressed in the heart, increases the sensitivity of heart mitochondria to the toxicity of doxorubicin. This study represents the first in vivo evidence of the antioxidant role of FtMt.
         datePublished:2014-04-13T00:00:00Z
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      headline:Mice lacking mitochondrial ferritin are more sensitive to doxorubicin-mediated cardiotoxicity
      description:Mitochondrial ferritin is a functional ferritin that localizes in the mitochondria. It is expressed in the testis, heart, brain, and cells with active respiratory activity. Its overexpression in cultured cells protected against oxidative damage and reduced cytosolic iron availability. However, no overt phenotype was described in mice with inactivation of the FtMt gene. Here, we used the doxorubicin model of cardiac injury in a novel strain of FtMt-null mice to investigate the antioxidant role of FtMt. These mice did not show any evident phenotype, but after acute treatment to doxorubicin, they showed enhanced mortality and altered heart morphology with fibril disorganization and severe mitochondrial damage. Signs of mitochondrial damage were present also in mock-treated FtMt−/− mice. The hearts of saline- and doxorubicin-treated FtMt−/− mice had higher thiobarbituric acid reactive substance levels, heme oxygenase 1 expression, and protein oxidation, but did not differ from FtMt+/+ in the cardiac damage marker B-type natriuretic peptide (BNP), ATP levels, and apoptosis. However, the autophagy marker LC3 was activated. The results show that the absence of FtMt, which is highly expressed in the heart, increases the sensitivity of heart mitochondria to the toxicity of doxorubicin. This study represents the first in vivo evidence of the antioxidant role of FtMt.
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         Ferritin
         Oxidative damage
         Mitochondria
         Doxorubicin
         Molecular Medicine
         Human Genetics
         Internal Medicine
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      name:Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy
      name:Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy
      name:Department of Molecular Biotechnology and Health Sciences, University of Torino, Torino, Italy
      name:Department of Molecular Biotechnology and Health Sciences, University of Torino, Torino, Italy
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      name:Department of Biomedical Sciences for Health, University of Milano, Milan, Italy

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