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  1. Artikel ; Online: ZIP14 is degraded in response to manganese exposure.

    Thompson, Khristy J / Wessling-Resnick, Marianne

    Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine

    2019  Band 32, Heft 6, Seite(n) 829–843

    Abstract: Manganese (Mn) is an essential element necessary for proper development and brain function. Circulating Mn levels are regulated by hepatobiliary clearance to limit toxic levels and prevent tissue deposition. To characterize mechanisms involved in ... ...

    Abstract Manganese (Mn) is an essential element necessary for proper development and brain function. Circulating Mn levels are regulated by hepatobiliary clearance to limit toxic levels and prevent tissue deposition. To characterize mechanisms involved in hepatocyte Mn uptake, polarized human HepaRG cells were used for this study. Western blot analysis and immunofluorescence microscopy showed the Mn transporter ZIP14 was expressed and localized to the basolateral surface of polarized HepaRG cells. HepaRG cells took up
    Mesh-Begriff(e) Cation Transport Proteins/metabolism ; Cell Survival/drug effects ; Cells, Cultured ; Humans ; Manganese/pharmacology ; Proteolysis/drug effects ; Temperature
    Chemische Substanzen Cation Transport Proteins ; SLC39A14 protein, human ; Manganese (42Z2K6ZL8P)
    Sprache Englisch
    Erscheinungsdatum 2019-09-20
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1112688-7
    ISSN 1572-8773 ; 0966-0844
    ISSN (online) 1572-8773
    ISSN 0966-0844
    DOI 10.1007/s10534-019-00216-1
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Manganese transport and toxicity in polarized WIF-B hepatocytes.

    Thompson, Khristy J / Hein, Jennifer / Baez, Andrew / Sosa, Jose Carlo / Wessling-Resnick, Marianne

    American journal of physiology. Gastrointestinal and liver physiology

    2018  Band 315, Heft 3, Seite(n) G351–G363

    Abstract: Manganese (Mn) toxicity arises from nutritional problems, community and occupational exposures, and genetic risks. Mn blood levels are controlled by hepatobiliary clearance. The goals of this study were to determine the cellular distribution of Mn ... ...

    Abstract Manganese (Mn) toxicity arises from nutritional problems, community and occupational exposures, and genetic risks. Mn blood levels are controlled by hepatobiliary clearance. The goals of this study were to determine the cellular distribution of Mn transporters in polarized hepatocytes, to establish an in vitro assay for hepatocyte Mn efflux, and to examine possible roles the Mn transporters would play in metal import and export. For these experiments, hepatocytoma WIF-B cells were grown for 12-14 days to achieve maximal polarity. Immunoblots showed that Mn transporters ZIP8, ZnT10, ferroportin (Fpn), and ZIP14 were present. Indirect immunofluorescence microscopy localized Fpn and ZIP14 to WIF-B cell basolateral domains whereas ZnT10 and ZIP8 associated with intracellular vesicular compartments. ZIP8-positive structures were distributed uniformly throughout the cytoplasm, but ZnT10-positive vesicles were adjacent to apical bile compartments. WIF-B cells were sensitive to Mn toxicity, showing decreased viability after 16 h exposure to >250 μM MnCl
    Mesh-Begriff(e) Animals ; Biological Transport/physiology ; Brefeldin A/metabolism ; Brefeldin A/pharmacology ; Cation Transport Proteins/metabolism ; Cell Line ; Cell Membrane/metabolism ; Cell Polarity ; Cytoplasmic Vesicles/metabolism ; Hepatocytes/drug effects ; Hepatocytes/metabolism ; Hepcidins/metabolism ; Hepcidins/pharmacology ; Humans ; Manganese/metabolism ; Manganese/toxicity ; Protein Synthesis Inhibitors/pharmacology
    Chemische Substanzen Cation Transport Proteins ; Hepcidins ; Protein Synthesis Inhibitors ; metal transporting protein 1 ; Brefeldin A (20350-15-6) ; Manganese (42Z2K6ZL8P)
    Sprache Englisch
    Erscheinungsdatum 2018-05-24
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 603840-2
    ISSN 1522-1547 ; 0193-1857
    ISSN (online) 1522-1547
    ISSN 0193-1857
    DOI 10.1152/ajpgi.00103.2018
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Manganese uptake and distribution in the brain after methyl bromide-induced lesions in the olfactory epithelia.

    Thompson, Khristy J / Molina, Ramon M / Donaghey, Thomas / Savaliya, Sandeep / Schwob, James E / Brain, Joseph D

    Toxicological sciences : an official journal of the Society of Toxicology

    2010  Band 120, Heft 1, Seite(n) 163–172

    Abstract: Manganese (Mn) is an essential nutrient with potential neurotoxic effects. Mn deposited in the nose is apparently transported to the brain through anterograde axonal transport, bypassing the blood-brain barrier. However, the role of the olfactory ... ...

    Abstract Manganese (Mn) is an essential nutrient with potential neurotoxic effects. Mn deposited in the nose is apparently transported to the brain through anterograde axonal transport, bypassing the blood-brain barrier. However, the role of the olfactory epithelial cells in Mn transport from the nasal cavity to the blood and brain is not well understood. We utilized the methyl bromide (MeBr) lesion model wherein the olfactory epithelium fully regenerates in a time-dependent and cell type-specific manner over the course of 6-8 weeks postinjury. We instilled (54)MnCl(2) intranasally at different recovery periods to study the role of specific olfactory epithelial cell types in Mn transport. (54)MnCl(2) was instilled at 2, 4, 7, 21, and 56 days post-MeBr treatment. (54)Mn concentrations in the blood were measured over the first 4-h period and in the brain and other tissues at 7 days postinstillation. Age-matched control rats were similarly studied at 2 and 56 days. Blood and tissue (54)Mn levels were reduced initially but returned to control values by day 7 post-MeBr exposure, coinciding with the reestablishment of sustentacular cells. Brain (54)Mn levels also decreased but returned to control levels only by 21 days, the period near the completion of neuronal regeneration/bulbar reinnervation. Our data show that Mn transport to the blood and brain temporally correlated with olfactory epithelial regeneration post-MeBr injury. We conclude that (1) sustentacular cells are necessary for Mn transport to the blood and (2) intact axonal projections are required for Mn transport from the nasal cavity to the olfactory bulb and brain.
    Mesh-Begriff(e) Administration, Intranasal ; Aging/blood ; Aging/metabolism ; Animals ; Brain/metabolism ; Chlorides/administration & dosage ; Chlorides/blood ; Chlorides/pharmacokinetics ; Hydrocarbons, Brominated/toxicity ; Injections, Intravenous ; Male ; Manganese Compounds/administration & dosage ; Manganese Compounds/blood ; Manganese Compounds/pharmacokinetics ; Olfactory Mucosa/drug effects ; Olfactory Mucosa/metabolism ; Olfactory Mucosa/pathology ; Olfactory Mucosa/physiology ; Rats ; Rats, Sprague-Dawley ; Regeneration/physiology ; Tissue Distribution
    Chemische Substanzen Chlorides ; Hydrocarbons, Brominated ; Manganese Compounds ; methyl bromide (9V42E1Z7B6) ; manganese chloride (QQE170PANO)
    Sprache Englisch
    Erscheinungsdatum 2010-12-20
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1420885-4
    ISSN 1096-0929 ; 1096-6080
    ISSN (online) 1096-0929
    ISSN 1096-6080
    DOI 10.1093/toxsci/kfq387
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Iron-responsive olfactory uptake of manganese improves motor function deficits associated with iron deficiency.

    Kim, Jonghan / Li, Yuan / Buckett, Peter D / Böhlke, Mark / Thompson, Khristy J / Takahashi, Masaya / Maher, Timothy J / Wessling-Resnick, Marianne

    PloS one

    2012  Band 7, Heft 3, Seite(n) e33533

    Abstract: Iron-responsive manganese uptake is increased in iron-deficient rats, suggesting that toxicity related to manganese exposure could be modified by iron status. To explore possible interactions, the distribution of intranasally-instilled manganese in ... ...

    Abstract Iron-responsive manganese uptake is increased in iron-deficient rats, suggesting that toxicity related to manganese exposure could be modified by iron status. To explore possible interactions, the distribution of intranasally-instilled manganese in control and iron-deficient rat brain was characterized by quantitative image analysis using T1-weighted magnetic resonance imaging (MRI). Manganese accumulation in the brain of iron-deficient rats was doubled after intranasal administration of MnCl(2) for 1- or 3-week. Enhanced manganese level was observed in specific brain regions of iron-deficient rats, including the striatum, hippocampus, and prefrontal cortex. Iron-deficient rats spent reduced time on a standard accelerating rotarod bar before falling and with lower peak speed compared to controls; unexpectedly, these measures of motor function significantly improved in iron-deficient rats intranasally-instilled with MnCl(2). Although tissue dopamine concentrations were similar in the striatum, dopamine transporter (DAT) and dopamine receptor D(1) (D1R) levels were reduced and dopamine receptor D(2) (D2R) levels were increased in manganese-instilled rats, suggesting that manganese-induced changes in post-synaptic dopaminergic signaling contribute to the compensatory effect. Enhanced olfactory manganese uptake during iron deficiency appears to be a programmed "rescue response" with beneficial influence on motor impairment due to low iron status.
    Mesh-Begriff(e) Administration, Intranasal ; Animals ; Brain/metabolism ; Brain/pathology ; Corpus Striatum/metabolism ; Dopamine/metabolism ; Dopamine Plasma Membrane Transport Proteins/metabolism ; Instillation, Drug ; Iron/deficiency ; Iron/metabolism ; Iron, Dietary ; Magnetic Resonance Imaging ; Manganese/administration & dosage ; Manganese/metabolism ; Motor Activity/physiology ; Olfactory Bulb/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Dopamine/metabolism
    Chemische Substanzen Dopamine Plasma Membrane Transport Proteins ; Iron, Dietary ; Receptors, Dopamine ; Manganese (42Z2K6ZL8P) ; Iron (E1UOL152H7) ; Dopamine (VTD58H1Z2X)
    Sprache Englisch
    Erscheinungsdatum 2012-03-30
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0033533
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Environmental mold and mycotoxin exposures elicit specific cytokine and chemokine responses.

    Rosenblum Lichtenstein, Jamie H / Hsu, Yi-Hsiang / Gavin, Igor M / Donaghey, Thomas C / Molina, Ramon M / Thompson, Khristy J / Chi, Chih-Lin / Gillis, Bruce S / Brain, Joseph D

    PloS one

    2015  Band 10, Heft 5, Seite(n) e0126926

    Abstract: Background: Molds can cause respiratory symptoms and asthma. We sought to use isolated peripheral blood mononuclear cells (PBMCs) to understand changes in cytokine and chemokine levels in response to mold and mycotoxin exposures and to link these levels ...

    Abstract Background: Molds can cause respiratory symptoms and asthma. We sought to use isolated peripheral blood mononuclear cells (PBMCs) to understand changes in cytokine and chemokine levels in response to mold and mycotoxin exposures and to link these levels with respiratory symptoms in humans. We did this by utilizing an ex vivo assay approach to differentiate mold-exposed patients and unexposed controls. While circulating plasma chemokine and cytokine levels from these two groups might be similar, we hypothesized that by challenging their isolated white blood cells with mold or mold extracts, we would see a differential chemokine and cytokine release.
    Methods and findings: Peripheral blood mononuclear cells (PBMCs) were isolated from blood from 33 patients with a history of mold exposures and from 17 controls. Cultured PBMCs were incubated with the most prominent Stachybotrys chartarum mycotoxin, satratoxin G, or with aqueous mold extract, ionomycin, or media, each with or without PMA. Additional PBMCs were exposed to spores of Aspergillus niger, Cladosporium herbarum and Penicillium chrysogenum. After 18 hours, cytokines and chemokines released into the culture medium were measured by multiplex assay. Clinical histories, physical examinations and pulmonary function tests were also conducted. After ex vivo PBMC exposures to molds or mycotoxins, the chemokine and cytokine profiles from patients with a history of mold exposure were significantly different from those of unexposed controls. In contrast, biomarker profiles from cells exposed to media alone showed no difference between the patients and controls.
    Conclusions: These findings demonstrate that chronic mold exposures induced changes in inflammatory and immune system responses to specific mold and mycotoxin challenges. These responses can differentiate mold-exposed patients from unexposed controls. This strategy may be a powerful approach to document immune system responsiveness to molds and other inflammation-inducing environmental agents.
    Mesh-Begriff(e) Adult ; Area Under Curve ; Biomarkers/blood ; Chemokines/blood ; Demography ; Environmental Exposure/analysis ; Female ; Fungi/drug effects ; Fungi/physiology ; Humans ; Ionomycin/toxicity ; Leukocytes, Mononuclear/metabolism ; Male ; Middle Aged ; Mycotoxins/toxicity ; Trichothecenes/toxicity
    Chemische Substanzen Biomarkers ; Chemokines ; Mycotoxins ; Trichothecenes ; satratoxin G (53126-63-9) ; Ionomycin (56092-81-0)
    Sprache Englisch
    Erscheinungsdatum 2015
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0126926
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  6. Artikel: Regulation, mechanisms and proposed function of ferritin translocation to cell nuclei.

    Thompson, Khristy J / Fried, Michael G / Ye, Zheng / Boyer, Phillip / Connor, James R

    Journal of cell science

    2002  Band 115, Heft Pt 10, Seite(n) 2165–2177

    Abstract: Ferritin is traditionally considered a cytoplasmic iron-storage protein, but recent reports indicate that it is also found in cell nuclei. Nuclear ferritin has been proposed to be involved in both the protection of DNA and the exacerbation of iron- ... ...

    Abstract Ferritin is traditionally considered a cytoplasmic iron-storage protein, but recent reports indicate that it is also found in cell nuclei. Nuclear ferritin has been proposed to be involved in both the protection of DNA and the exacerbation of iron-induced oxidative damage to DNA. We demonstrate that H-rich ferritin is present in the nucleus of human astrocytoma tumor cells. To study the mechanism and regulation of ferritin translocation to the nucleus, we developed a cell culture model using SW1088 human astrocytoma cells. Changes in cellular iron levels, cytokine treatments and hydrogen peroxide exposure affected the distribution of ferritin between the cytosol and the nucleus. Ferritin enters the nucleus via active transport through the nuclear pore and does not require NLS-bearing cytosolic factors for transport. Furthermore, H-rich ferritin is preferred over L-rich ferritin for uptake into the nucleus. Whole cell crosslinking studies revealed that ferritin is associated with DNA. Ferritin protected DNA from iron-induced oxidative damage in both in vitro and in cell culture models. These results strongly suggest a novel role for ferritin in nuclear protection. This work should lead to novel characterization of ferritin functions in the context of genomic stability and may have unparalleled biological significance in terms of the accessibility of metals to DNA. The knowledge generated as a result of these studies will also improve our understanding of iron-induced damage of nuclear constituents.
    Mesh-Begriff(e) Active Transport, Cell Nucleus/drug effects ; Astrocytoma/metabolism ; Astrocytoma/pathology ; Cell Nucleus/drug effects ; Cell Nucleus/metabolism ; Cytokines/pharmacology ; DNA/metabolism ; DNA Damage ; Ferritins/metabolism ; Humans ; Hydrogen Peroxide/pharmacology ; Iron/metabolism ; Iron/pharmacology ; Tumor Cells, Cultured
    Chemische Substanzen Cytokines ; DNA (9007-49-2) ; Ferritins (9007-73-2) ; Hydrogen Peroxide (BBX060AN9V) ; Iron (E1UOL152H7)
    Sprache Englisch
    Erscheinungsdatum 2002-05-15
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 2993-2
    ISSN 1477-9137 ; 0021-9533
    ISSN (online) 1477-9137
    ISSN 0021-9533
    DOI 10.1242/jcs.115.10.2165
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel: Manganese and iron transport across pulmonary epithelium.

    Heilig, Elizabeth A / Thompson, Khristy J / Molina, Ramon M / Ivanov, Alexander R / Brain, Joseph D / Wessling-Resnick, Marianne

    American journal of physiology. Lung cellular and molecular physiology

    2006  Band 290, Heft 6, Seite(n) L1247–59

    Abstract: Pathways mediating pulmonary metal uptake remain unknown. Because absorption of iron and manganese could involve similar mechanisms, transferrin (Tf) and transferrin receptor (TfR) expression in rat lungs was examined. Tf mRNA was detected in bronchial ... ...

    Abstract Pathways mediating pulmonary metal uptake remain unknown. Because absorption of iron and manganese could involve similar mechanisms, transferrin (Tf) and transferrin receptor (TfR) expression in rat lungs was examined. Tf mRNA was detected in bronchial epithelium, type II alveolar cells, macrophages, and bronchus-associated lymphoid tissue (BALT). Tf protein levels in lung and bronchoalveolar lavage fluid did not change in iron deficiency despite increased plasma levels, suggesting that lung Tf concentrations are regulated by local synthesis in a manner independent of body iron status. Iron oxide exposure upregulated Tf mRNA in bronchial and alveolar epithelium, macrophages, and BALT, but protein was not significantly increased. In contrast, TfR mRNA and protein were both upregulated by iron deficiency. To examine potential interactions with lung Tf, rats were intratracheally instilled with (54)Mn or (59)Fe. Unlike (59)Fe, interactions between (54)Mn and Tf in lung fluid were not detected. Absorption of intratracheally instilled (54)Mn from the lungs to the blood was unimpaired in Belgrade rats homozygous for the functionally defective G185R allele of divalent metal transporter-1, indicating that this transporter is also not involved in pulmonary manganese absorption. Pharmacological studies of (54)Mn uptake by A549 cells suggest that metal uptake by type II alveolar epithelial cells is associated with activities of both L-type Ca(2+) channels and TRPM7, a member of the transient receptor potential melastatin subfamily. These results demonstrate that iron and manganese are absorbed by the pulmonary epithelium through different pathways and reveal the potential role for nonselective calcium channels in lung metal clearance.
    Mesh-Begriff(e) Animals ; Base Sequence ; Biological Transport ; DNA Primers ; In Situ Hybridization ; Iron/metabolism ; Lung/cytology ; Lung/physiology ; Male ; Manganese/metabolism ; RNA, Messenger/genetics ; Rats ; Rats, Sprague-Dawley ; Receptors, Transferrin/genetics ; Respiratory Mucosa/cytology ; Respiratory Mucosa/physiology ; Transferrin/genetics
    Chemische Substanzen DNA Primers ; RNA, Messenger ; Receptors, Transferrin ; Transferrin ; Manganese (42Z2K6ZL8P) ; Iron (E1UOL152H7)
    Sprache Englisch
    Erscheinungsdatum 2006-01-20
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00450.2005
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