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  1. AU="Perrier, Prunelle"
  2. AU=Chisari Emanuele AU=Chisari Emanuele
  3. AU="Sibiya, Maureen Nokuthula"
  4. AU="Gokce, Emine"
  5. AU="Muth, Christiane"
  6. AU="Cüneyt Orhan Kara"
  7. AU="Arnberg, Fabian"
  8. AU="Rana, Shubham"
  9. AU="Hugen, Cory M"
  10. AU="Andres M. Rubiano"
  11. AU="Nicole Matejka"
  12. AU="Nunes, Pedro M. Sales"
  13. AU="Sánchez-Montero, María Teresa"
  14. AU="Jiexin Zhang"
  15. AU=Mladinic M
  16. AU="Canfarotta, Michael W"
  17. AU="Merani, Shaheed"
  18. AU="Tarver, James E"
  19. AU=Wirestam Lina
  20. AU="Karen Martz"
  21. AU="Yadav, Kanhaiya L."
  22. AU="Girmay, Tigisty"
  23. AU="Hain, Sofia"
  24. AU="de Kler, R C F"
  25. AU="Veness, R."

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  1. Artikel ; Online: The hepatokine FGL1 regulates hepcidin and iron metabolism during anemia in mice by antagonizing BMP signaling.

    Sardo, Ugo / Perrier, Prunelle / Cormier, Kevin / Sotin, Manon / Personnaz, Jean / Medjbeur, Thanina / Desquesnes, Aurore / Cannizzo, Lisa / Ruiz-Martinez, Marc / Thevenin, Julie / Billoré, Benjamin / Jung, Grace / Abboud, Elise / Peyssonnaux, Carole / Nemeth, Elizabeta / Ginzburg, Yelena Z / Ganz, Tomas / Kautz, Léon

    Blood

    2024  Band 143, Heft 13, Seite(n) 1282–1292

    Abstract: Abstract: As a functional component of erythrocyte hemoglobin, iron is essential for oxygen delivery to all tissues in the body. The liver-derived peptide hepcidin is the master regulator of iron homeostasis. During anemia, the erythroid hormone ... ...

    Abstract Abstract: As a functional component of erythrocyte hemoglobin, iron is essential for oxygen delivery to all tissues in the body. The liver-derived peptide hepcidin is the master regulator of iron homeostasis. During anemia, the erythroid hormone erythroferrone regulates hepcidin synthesis to ensure the adequate supply of iron to the bone marrow for red blood cell production. However, mounting evidence suggested that another factor may exert a similar function. We identified the hepatokine fibrinogen-like 1 (FGL1) as a previously undescribed suppressor of hepcidin that is induced in the liver in response to hypoxia during the recovery from anemia, and in thalassemic mice. We demonstrated that FGL1 is a potent suppressor of hepcidin in vitro and in vivo. Deletion of Fgl1 in mice results in higher hepcidin levels at baseline and after bleeding. FGL1 exerts its activity by directly binding to bone morphogenetic protein 6 (BMP6), thereby inhibiting the canonical BMP-SMAD signaling cascade that controls hepcidin transcription.
    Mesh-Begriff(e) Mice ; Animals ; Hepcidins/genetics ; Hepcidins/metabolism ; Anemia/genetics ; Anemia/metabolism ; Iron/metabolism ; Liver/metabolism ; Bone Morphogenetic Protein 6/genetics ; Bone Morphogenetic Protein 6/metabolism ; Homeostasis
    Chemische Substanzen Hepcidins ; Iron (E1UOL152H7) ; Bone Morphogenetic Protein 6
    Sprache Englisch
    Erscheinungsdatum 2024-01-17
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2023022724
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: The hepatokine FGL1 regulates hepcidin and iron metabolism during the recovery from hemorrhage-induced anemia in mice.

    Sardo, Ugo / Perrier, Prunelle / Cormier, Kevin / Sotin, Manon / Desquesnes, Aurore / Cannizzo, Lisa / Ruiz-Martinez, Marc / Thevenin, Julie / Billoré, Benjamin / Jung, Grace / Abboud, Elise / Peyssonnaux, Carole / Nemeth, Elizabeta / Ginzburg, Yelena Z / Ganz, Tomas / Kautz, Léon

    bioRxiv : the preprint server for biology

    2023  

    Abstract: As a functional component of erythrocyte hemoglobin, iron is essential for oxygen delivery to all tissues in the body. The liver-derived peptide hepcidin is the master regulator of iron homeostasis. During anemia, the erythroid hormone erythroferrone ... ...

    Abstract As a functional component of erythrocyte hemoglobin, iron is essential for oxygen delivery to all tissues in the body. The liver-derived peptide hepcidin is the master regulator of iron homeostasis. During anemia, the erythroid hormone erythroferrone regulates hepcidin synthesis to ensure adequate supply of iron to the bone marrow for red blood cells production. However, mounting evidence suggested that another factor may exert a similar function. We identified the hepatokine FGL1 as a previously undescribed suppressor of hepcidin that is induced in the liver in response to hypoxia during the recovery from anemia and in thalassemic mice. We demonstrated that FGL1 is a potent suppressor of hepcidin
    Key points: 1/ FGL1 regulates iron metabolism during the recovery from anemia.
    Sprache Englisch
    Erscheinungsdatum 2023-04-06
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2023.04.06.535920
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Dietary Amino Acid Source Elicits Sex-Specific Metabolic Response to Diet-Induced NAFLD in Mice.

    Rives, Clémence / Martin, Céline Marie Pauline / Evariste, Lauris / Polizzi, Arnaud / Huillet, Marine / Lasserre, Frédéric / Alquier-Bacquie, Valérie / Perrier, Prunelle / Gomez, Jelskey / Lippi, Yannick / Naylies, Claire / Levade, Thierry / Sabourdy, Frédérique / Remignon, Hervé / Fafournoux, Pierre / Chassaing, Benoit / Loiseau, Nicolas / Guillou, Hervé / Ellero-Simatos, Sandrine /
    Gamet-Payrastre, Laurence / Fougerat, Anne

    Molecular nutrition & food research

    2023  Band 68, Heft 1, Seite(n) e2300491

    Abstract: Scope: Non-alcoholic fatty liver disease (NAFLD) is a sexually dimorphic disease influenced by dietary factors. Here, the metabolic and hepatic effects of dietary amino acid (AA) source is assessed in Western diet (WD)-induced NAFLD in male and female ... ...

    Abstract Scope: Non-alcoholic fatty liver disease (NAFLD) is a sexually dimorphic disease influenced by dietary factors. Here, the metabolic and hepatic effects of dietary amino acid (AA) source is assessed in Western diet (WD)-induced NAFLD in male and female mice.
    Methods and results: The AA source is either casein or a free AA mixture mimicking the composition of casein. As expected, males fed a casein-based WD display glucose intolerance, fasting hyperglycemia, and insulin-resistance and develop NAFLD associated with changes in hepatic gene expression and microbiota dysbiosis. In contrast, males fed the AA-based WD show no steatosis, a similar gene expression profile as males fed a control diet, and a distinct microbiota composition compared to males fed a casein-based WD. Females are protected against WD-induced liver damage, hepatic gene expression, and gut microbiota changes regardless of the AA source.
    Conclusions: Free dietary AA intake prevents the unhealthy metabolic outcomes of a WD preferentially in male mice.
    Mesh-Begriff(e) Male ; Female ; Animals ; Mice ; Non-alcoholic Fatty Liver Disease/etiology ; Non-alcoholic Fatty Liver Disease/prevention & control ; Caseins/pharmacology ; Liver/metabolism ; Diet, Western/adverse effects ; Amino Acids/metabolism ; Mice, Inbred C57BL ; Diet, High-Fat
    Chemische Substanzen Caseins ; Amino Acids
    Sprache Englisch
    Erscheinungsdatum 2023-10-27
    Erscheinungsland Germany
    Dokumenttyp Journal Article
    ZDB-ID 2160372-8
    ISSN 1613-4133 ; 1613-4125
    ISSN (online) 1613-4133
    ISSN 1613-4125
    DOI 10.1002/mnfr.202300491
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: A fully human anti-BMP6 antibody reduces the need for erythropoietin in rodent models of the anemia of chronic disease.

    Petzer, Verena / Tymoszuk, Piotr / Asshoff, Malte / Carvalho, Joana / Papworth, Jonathan / Deantonio, Cecilia / Bayliss, Luke / Wake, Matthew Stephen / Seifert, Markus / Brigo, Natascha / Valente de Souza, Lara / Hilbe, Richard / Grubwieser, Philipp / Demetz, Egon / Dichtl, Stefanie / Volani, Chiara / Berger, Sylvia / Böhm, Felix / Hoffmann, Alexander /
    Pfeifhofer-Obermair, Christa / von Raffay, Laura / Sopper, Sieghart / Arndt, Stephanie / Bosserhoff, Anja / Kautz, Léon / Perrier, Prunelle / Nairz, Manfred / Wolf, Dominik / Weiss, Guenter / Germaschewski, Volker / Theurl, Igor

    Blood

    2020  Band 136, Heft 9, Seite(n) 1080–1090

    Abstract: Recombinant erythropoietin (EPO) and iron substitution are a standard of care for treatment of anemias associated with chronic inflammation, including anemia of chronic kidney disease. A black box warning for EPO therapy and concerns about negative side ... ...

    Abstract Recombinant erythropoietin (EPO) and iron substitution are a standard of care for treatment of anemias associated with chronic inflammation, including anemia of chronic kidney disease. A black box warning for EPO therapy and concerns about negative side effects related to high-dose iron supplementation as well as the significant proportion of patients becoming EPO resistant over time explains the medical need to define novel strategies to ameliorate anemia of chronic disease (ACD). As hepcidin is central to the iron-restrictive phenotype in ACD, therapeutic approaches targeting hepcidin were recently developed. We herein report the therapeutic effects of a fully human anti-BMP6 antibody (KY1070) either as monotherapy or in combination with Darbepoetin alfa on iron metabolism and anemia resolution in 2 different, well-established, and clinically relevant rodent models of ACD. In addition to counteracting hepcidin-driven iron limitation for erythropoiesis, we found that the combination of KY1070 and recombinant human EPO improved the erythroid response compared with either monotherapy in a qualitative and quantitative manner. Consequently, the combination of KY1070 and Darbepoetin alfa resulted in an EPO-sparing effect. Moreover, we found that suppression of hepcidin via KY1070 modulates ferroportin expression on erythroid precursor cells, thereby lowering potentially toxic-free intracellular iron levels and by accelerating erythroid output as reflected by increased maturation of erythrocyte progenitors. In summary, we conclude that treatment of ACD, as a highly complex disease, becomes more effective by a multifactorial therapeutic approach upon mobilization of endogenous iron deposits and stimulation of erythropoiesis.
    Mesh-Begriff(e) Anemia/drug therapy ; Anemia/etiology ; Anemia/therapy ; Animals ; Antibodies, Monoclonal/administration & dosage ; Antibodies, Monoclonal/immunology ; Antibodies, Monoclonal/therapeutic use ; Arthritis/chemically induced ; Arthritis/complications ; Bone Marrow/metabolism ; Bone Morphogenetic Protein 6/antagonists & inhibitors ; Bone Morphogenetic Protein 6/immunology ; Cation Transport Proteins/metabolism ; Cytokines/blood ; Darbepoetin alfa/administration & dosage ; Darbepoetin alfa/therapeutic use ; Dose-Response Relationship, Drug ; Drug Synergism ; Erythropoietin/pharmacology ; Erythropoietin/therapeutic use ; Hep G2 Cells ; Humans ; Iron/metabolism ; Mice ; Muscle Proteins/blood ; Polysaccharides, Bacterial/toxicity ; Random Allocation ; Recombinant Proteins/immunology ; Renal Insufficiency, Chronic/complications
    Chemische Substanzen Antibodies, Monoclonal ; BMP6 protein, human ; Bmp6 protein, mouse ; Bmp6 protein, rat ; Bone Morphogenetic Protein 6 ; Cation Transport Proteins ; Cytokines ; Erfe protein, mouse ; Muscle Proteins ; Polysaccharides, Bacterial ; Recombinant Proteins ; metal transporting protein 1 ; streptococcal polysaccharide group A ; Erythropoietin (11096-26-7) ; Darbepoetin alfa (15UQ94PT4P) ; Iron (E1UOL152H7)
    Sprache Englisch
    Erscheinungsdatum 2020-05-21
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2019004653
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: A variant erythroferrone disrupts iron homeostasis in

    Bondu, Sabrina / Alary, Anne-Sophie / Lefèvre, Carine / Houy, Alexandre / Jung, Grace / Lefebvre, Thibaud / Rombaut, David / Boussaid, Ismael / Bousta, Abderrahmane / Guillonneau, François / Perrier, Prunelle / Alsafadi, Samar / Wassef, Michel / Margueron, Raphaël / Rousseau, Alice / Droin, Nathalie / Cagnard, Nicolas / Kaltenbach, Sophie / Winter, Susann /
    Kubasch, Anne-Sophie / Bouscary, Didier / Santini, Valeria / Toma, Andrea / Hunault, Mathilde / Stamatoullas, Aspasia / Gyan, Emmanuel / Cluzeau, Thomas / Platzbecker, Uwe / Adès, Lionel / Puy, Hervé / Stern, Marc-Henri / Karim, Zoubida / Mayeux, Patrick / Nemeth, Elizabeta / Park, Sophie / Ganz, Tomas / Kautz, Léon / Kosmider, Olivier / Fontenay, Michaëla

    Science translational medicine

    2019  Band 11, Heft 500

    Abstract: Myelodysplastic syndromes (MDS) with ring sideroblasts are hematopoietic stem cell disorders with erythroid dysplasia and mutations in ... ...

    Abstract Myelodysplastic syndromes (MDS) with ring sideroblasts are hematopoietic stem cell disorders with erythroid dysplasia and mutations in the
    Mesh-Begriff(e) Alternative Splicing/drug effects ; Alternative Splicing/genetics ; Amino Acid Sequence ; Animals ; Blood Transfusion ; Cell Line ; Cell Lineage/drug effects ; Cell Survival/drug effects ; Clone Cells ; Erythroid Cells/drug effects ; Erythroid Cells/metabolism ; Hepcidins/metabolism ; Homeostasis/drug effects ; Humans ; Iron/metabolism ; Lenalidomide/pharmacology ; Mice ; Mutation/genetics ; Myelodysplastic Syndromes/blood ; Myelodysplastic Syndromes/genetics ; Peptide Hormones/blood ; Peptide Hormones/chemistry ; Peptide Hormones/genetics ; Peptide Hormones/metabolism ; Phosphoproteins/genetics ; Protein Biosynthesis/drug effects ; RNA Splice Sites/genetics ; RNA Splicing Factors/genetics ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Up-Regulation/drug effects ; Up-Regulation/genetics
    Chemische Substanzen Erfe protein, human ; Hepcidins ; Peptide Hormones ; Phosphoproteins ; RNA Splice Sites ; RNA Splicing Factors ; RNA, Messenger ; SF3B1 protein, human ; Iron (E1UOL152H7) ; Lenalidomide (F0P408N6V4)
    Sprache Englisch
    Erscheinungsdatum 2019-07-10
    Erscheinungsland United States
    Dokumenttyp Clinical Trial ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2518854-9
    ISSN 1946-6242 ; 1946-6234
    ISSN (online) 1946-6242
    ISSN 1946-6234
    DOI 10.1126/scitranslmed.aav5467
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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