High erythroferrone expression in CD71
Adult
Aged
Aged, 80 and over
Antigens, CD
/ analysis
Erythroid Precursor Cells
/ chemistry
Female
Growth Differentiation Factor 15
/ biosynthesis
Humans
Kaplan-Meier Estimate
Male
Middle Aged
Myelodysplastic Syndromes
/ metabolism
Peptide Hormones
/ biosynthesis
Phosphoproteins
/ genetics
Proportional Hazards Models
RNA Splicing Factors
/ genetics
Receptors, Transferrin
/ analysis
Treatment Outcome
Young Adult
erythroferrone
erythroid progenitors
iron metabolism
iron overload
myelodysplastic syndromes
Journal
British journal of haematology
ISSN: 1365-2141
Titre abrégé: Br J Haematol
Pays: England
ID NLM: 0372544
Informations de publication
Date de publication:
03 2021
03 2021
Historique:
received:
11
10
2020
accepted:
14
12
2020
pubmed:
25
1
2021
medline:
10
8
2021
entrez:
24
1
2021
Statut:
ppublish
Résumé
Ineffective erythropoiesis and iron overload are common in myelodysplastic syndromes (MDS). Erythroferrone (ERFE) and growth/differentiation factor 15 (GDF15) are two regulators of iron homeostasis produced by erythroid progenitors. Elevated systemic levels of ERFE and GDF15 in MDS are associated with dysregulated iron metabolism and iron overload, which is especially pronounced in MDS with SF3B1 gene mutations. However, the role of ERFE and GDF15 in MDS pathogenesis and their influence on disease progression are largely unknown. Here, we analyzed the expression of ERFE and GDF15 in CD71
Substances chimiques
Antigens, CD
0
CD71 antigen
0
Erfe protein, human
0
GDF15 protein, human
0
Growth Differentiation Factor 15
0
Peptide Hormones
0
Phosphoproteins
0
RNA Splicing Factors
0
Receptors, Transferrin
0
SF3B1 protein, human
0
Types de publication
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
879-891Subventions
Organisme : Deutsche Forschungsgemeinschaft (DFG)
ID : 817/5-2
Organisme : Deutsche Forschungsgemeinschaft (DFG)
ID : FOR2033
Organisme : Deutsche Forschungsgemeinschaft (DFG)
ID : NICHEM
Organisme : Gutermuth Foundation
Organisme : H.W. & J. Hector foundation (Weinheim)
ID : M83
Organisme : Dr. Rolf M. Schwiete Foundation (Mannheim)
ID : 20/2016
Organisme : German José-Carreras-Foundation
ID : DJCLSH03/01
Informations de copyright
© 2021 The Authors. British Journal of Haematology published by British Society for Haematology and John Wiley & Sons Ltd.
Références
Gattermann N. Iron overload in myelodysplastic syndromes (MDS). Int J Hematol. 2018;107(1):55-63.
Gupta R, Musallam KM, Taher AT, Rivella S. Ineffective erythropoiesis: anemia and iron overload. Hematol/Oncol Clin. 2018;32(2):213-21.
Finkenstedt A, Bianchi P, Theurl I, Vogel W, Witcher DR, Wroblewski VJ, et al. Regulation of iron metabolism through GDF15 and hepcidin in pyruvate kinase deficiency. Br J Haematol. 2009;144(5):789-93.
Kautz L, Jung G, Valore EV, Rivella S, Nemeth E, Ganz T. Identification of erythroferrone as an erythroid regulator of iron metabolism. Nat Genet. 2014;46(7):678-84.
Wang C, Fang Z, Zhu Z, Liu J, Chen H. Reciprocal regulation between hepcidin and erythropoiesis and its therapeutic application in erythroid disorders. Exp Hematol. 2017;52:24-31.
Lawen A. Is erythroferrone finally the long sought-after systemic erythroid regulator of iron? World J Biol Chem. 2015;6(3):78.
Seldin MM, Peterson JM, Byerly MS, Wei Z, Wong GW. Myonectin (CTRP15), a novel myokine that links skeletal muscle to systemic lipid homeostasis. J Biol Chem. 2012;287(15):11968-80.
Bondu S, Alary A-S, Lefèvre C, Houy A, Jung G, Lefebvre T, et al. A variant erythroferrone disrupts iron homeostasis in SF3B1-mutated myelodysplastic syndrome. Sci Transl Med. 2019;11(500):eaav5467.
Camaschella C, Pagani A, Nai A, Silvestri L. The mutual control of iron and erythropoiesis. Int J Lab Hematol. 2016;38:20-6.
Cui R, Gale RP, Zhu G, Xu Z, Qin T, Zhang Y, et al. Serum iron metabolism and erythropoiesis in patients with myelodysplastic syndrome not receiving RBC transfusions. Leuk Res. 2014;38(5):545-50.
Park S, Kosmider O, Maloisel F, Drenou B, Chapuis N, Lefebvre T, et al. Dyserythropoiesis evaluated by the RED score and hepcidin: ferritin ratio predicts response to erythropoietin in lower-risk myelodysplastic syndromes. Haematologica. 2019;104(3):497-504.
Tanno T, Bhanu NV, Oneal PA, Goh S-H, Staker P, Lee YT, et al. High levels of GDF15 in thalassemia suppress expression of the iron regulatory protein hepcidin. Nat Med. 2007;13(9):1096-101.
Ganz T. Erythropoietic regulators of iron metabolism. Free Radic Biol Med. 2019;133:69-74.
Santini V, Girelli D, Sanna A, Martinelli N, Duca L, Campostrini N, et al. Hepcidin levels and their determinants in different types of myelodysplastic syndromes. PLoS One. 2011;6(8):e23109.
Temraz S, Santini V, Musallam K, Taher A. Iron overload and chelation therapy in myelodysplastic syndromes. Crit Rev Oncol/Hematol. 2014;91(1):64-73.
Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2− ΔΔCT method. Methods. 2001;25(4):402-8.
Mori Y, Chen JY, Pluvinage JV, Seita J, Weissman IL. Prospective isolation of human erythroid lineage-committed progenitors. Proc Natl Acad Sci USA. 2015;112(31):9638-43.
Dinh HQ, Eggert T, Meyer MA, Zhu YP, Olingy CE, Llewellyn R, et al. Coexpression of CD71 and CD117 identifies an early unipotent neutrophil progenitor population in human bone marrow. Immunity. 2020;53(2):319-34. e6.
Beguin Y. Soluble transferrin receptor for the evaluation of erythropoiesis and iron status. Clin Chim Acta. 2003;329(1-2):9-22.
Dong HY, Wilkes S, Yang H. CD71 is selectively and ubiquitously expressed at high levels in erythroid precursors of all maturation stages: a comparative immunochemical study with glycophorin A and hemoglobin A. Am J Surg Pathol. 2011;35(5):723-32.
Marsee DK, Pinkus GS, Yu H. CD71 (transferrin receptor) an effective marker for erythroid precursors in bone marrow biopsy specimens. Am J Clin Pathol. 2010;134(3):429-35.
Bejar R. Clinical and genetic predictors of prognosis in myelodysplastic syndromes. Haematologica. 2014;99(6):956-64.
Malcovati L, Stevenson K, Papaemmanuil E, Neuberg D, Bejar R, Boultwood J, et al. SF3B1-mutant myelodysplastic syndrome as a distinct disease subtype-A Proposal of the International Working Group for the Prognosis of Myelodysplastic Syndromes (IWG-PM). Blood. 2020;136(2):157-70.
Ganz T, Jung G, Naeim A, Ginzburg Y, Pakbaz Z, Walter PB, et al. Immunoassay for human serum erythroferrone. Blood. 2017;130(10):1243-6.
Kautz L, Jung G, Du X, Gabayan V, Chapman J, Nasoff M, et al. Erythroferrone contributes to hepcidin suppression and iron overload in a mouse model of β-thalassemia. Blood. 2015;126(17):2031-7.
Huang Y, Liu R, Wei X, Liu J, Pan L, Yang G, et al. Erythropoiesis and iron homeostasis in non-transfusion-dependent thalassemia patients with extramedullary hematopoiesis. Biomed Res Int. 2019;2019:4504302.
Miura S, Kobune M, Horiguchi H, Kikuchi S, Iyama S, Murase K, et al. EPO-R+ myelodysplastic cells with ring sideroblasts produce high erythroferrone levels to reduce hepcidin expression in hepatic cells. Blood Cells Mol Dis. 2019;78:1-8.
Bootcov MR, Bauskin AR, Valenzuela SM, Moore AG, Bansal M, He XY, et al. MIC-1, a novel macrophage inhibitory cytokine, is a divergent member of the TGF-β superfamily. Proc Natl Acad Sci USA. 1997;94(21):11514-9.
Ha G, De Torres F, Arouche N, Benzoubir N, Ferratge S, Hatem E, et al. GDF15 secreted by senescent endothelial cells improves vascular progenitor cell functions. PLoS One. 2019;14(5):e0216602.
Kim J, Kosak J, Kim J, Kissling G, Germolec D, Zeldin D, et al. NAG-1/GDF15 transgenic mouse has less white adipose tissue and a reduced inflammatory response. Mediators Inflamm. 2013;2013:641851.
Li M, Song K, Huang X, Fu S, Zeng Q. GDF15 prevents LPS and D-galactosamine-induced inflammation and acute liver injury in mice. Int J Mol Med. 2018;42(3):1756-64.
Otaka N, Shibata R, Ohashi K, Uemura Y, Kambara T, Enomoto T, et al. Myonectin is an exercise-induced myokine that protects the heart from ischemia-reperfusion injury. Circ Res. 2018;123(12):1326-38.
Quandt D, Fiedler E, Boettcher D, Marsch WC, Seliger B. B7-h4 expression in human melanoma: its association with patients' survival and antitumor immune response. Clin Cancer Res. 2011;17(10):3100-11.
Ratnam NM, Peterson JM, Talbert EE, Ladner KJ, Rajasekera PV, Schmidt CR, et al. NF-κB regulates GDF-15 to suppress macrophage surveillance during early tumor development. J Clin Investig. 2017;127(10):3796-809.
Luan HH, Wang A, Hilliard BK, Carvalho F, Rosen CE, Ahasic AM, et al. GDF15 is an inflammation-induced central mediator of tissue tolerance. Cell. 2019;178(5):1231-44. e11.