Dergiler / Turkish Journal of Medical Sciences / 2019 / Cilt: 49 - Sayı: 1

The role of hepcidin, GDF15, and mitoferrin-1 in iron metabolism of polycythemia vera and essential thrombocytosis patients

Sayfa
74–80
Yayın Tarihi
2022-11-05
DOI
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⚡ TL;DR(1 Cümlede Hızlı Çıkarım)

It can be hypothesized that similar hepcidin levels in patients and controls and low mfrn-1levels in patients may be a defense mechanism against erythroid activity and thromboembolic complications.

📌 3 Maddede Bu Makale

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Amaç & Hipotez:Background/aim: GDF15, hepcidin and mitoferrin-1 (mfrn-1) are proteins involved in systemic iron regulation.
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Temel Bulgular & Veri:There are no studiesin the literature demonstrating the serum mfrn-1 levels in polycythemia vera (PV) and essential thrombocythemia (ET) patients.
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Sonuç & Katkı:It can be hypothesized that similar hepcidin levels in patients and controls and low mfrn-1levels in patients may be a defense mechanism against erythroid activity and thromboembolic complications.
🔬Tür:Araştırma Makalesi
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Alan Parametreleri

Abstract

Background/aim: GDF15, hepcidin and mitoferrin-1 (mfrn-1) are proteins involved in systemic iron regulation. There are no studiesin the literature demonstrating the serum mfrn-1 levels in polycythemia vera (PV) and essential thrombocythemia (ET) patients. Theaim of this study was to investigate GDF15, hepcidin and mfrn-1 levels in PV and ET patients.Materials and methods: Ten PV, 17 ET patients, and 27 healthy controls (HCs) were enrolled. GDF15, hepcidin and mfrn-1 values weremeasured with enzyme-linked immunosorbent assay (ELISA).Results: GDF15 levels were higher in the myeloproliferative neoplasm (MPN) group (P = 0.002). Hepcidin levels were not differentbetween MPN patients and HCs. The mfrn-1 levels were lower in MPN patients (P = 0.039). Hepcidin, GDF15, and mfrn-1 levels werenot different between PV and ET patients. mfrn-1 levels were lower in ET patients than HCs (P = 0.038).Conclusion: Increased erythropoiesis in MPNs may lead to high GDF15 levels in these patients. However, hepcidin was not suppresseddespite the increased GDF15 levels and erythropoiesis in these patients. Decrease in mfrn-1 in MPNs can be the result of its increasedturnover due to increased myelopoiesis. It can be hypothesized that similar hepcidin levels in patients and controls and low mfrn-1levels in patients may be a defense mechanism against erythroid activity and thromboembolic complications.

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Bu Makaleye Atıf Yap

ERALDEMİR, C., DEMİRSOY, E. T., ATEŞOĞLU, E. B., ÖZSOY, Ö. D., HACIHANEFİOĞLU, A., GEDÜK, A., MEHTAP, Ö., TARKUN, P., ALBAYRAK, C. (2022). The role of hepcidin, GDF15, and mitoferrin-1 in iron metabolism of polycythemia vera and essential thrombocytosis patients. Turkish Journal of Medical Sciences, Cilt: 49 - Sayı: 1, 74–80. https://ajindex.com/articles/609987

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Kaynakça (16)

  1. Hoffman R, Baker KR, Prchal JT. The polycythemias. In: Hoffman R, Benz EJ, Shattil SJ, editors. Hematology: Basic Principles and Practice. 6th ed. Philadelphia, PA, USA: Saunders, Elsevier; 2005. pp. 1209-1291
  2. Tefferi A, Vainchenker W. Myeloproliferative neoplasms: molecular pathology, essential clinical understanding, and treatment strategies. J Clin Oncol 2011; 29: 573-582
  3. Tefferi A. JAK and MPL mutations in myeloid malignancies. Leukemia Lymphoma 2008; 49: 388-397
  4. Tefferi A. JAK2 mutations and clinical practice in myeloproliferative neoplasms. Cancer J 2007; 13: 366-371
  5. Josef T, Prchal FJ. Polycythemia vera. In: Lichtman M, Kaushansky K, Beutler E, Seligsohn U, Kipps T, Prchal FJ, editors. Williams Hematology. 8th ed. New York, NY, USA: McGraw-Hill; 2010. pp. 1919-1943
  6. Nemeth E, Ganz T. The role of hepcidin in iron metabolism. Acta Haematol 2009; 122: 78-86
  7. Tanno T, Noel P, Miller JL. Growth differentiation factor 15 in erythroid health and disease. Curr Opin Hematol 2010; 17: 184-90
  8. Nancy CA. ABCs of erythroid mitochondrial iron uptake. P Natl Acad Sci USA 2009; 106: 16012-16013
  9. Shaw GC, Cope JJ, Li L, Corson K, Hersey C, Ackermann GE, Gwynn B, Lambert AJ, Wingert RA, Traver D et al. Mitoferrin is essential for erythroid iron assimilation. Nature 2006; 440: 96-100
  10. Paradkar PN, Zumbrennen KB, Paw BH, Ward DM, Kaplan J. Regulation of mitochondrial iron import through differential turnover of mitoferrin 1 and mitoferrin 2. Mol Cell Biol 2009; 29: 1007-1016
  11. Chen W, Paradkar PN, Li L, Pierce EL, Langer NB, TakahashiMakise N, Hyde BB, Shirihai OS, Ward DM, Kaplan J et al. Abcb10 physically interacts with mitoferrin-1 (Slc25a37) to enhance its stability and function in the erythroid mitochondria. P Natl Acad Sci USA 2009; 106: 16263-16268
  12. Chen W, Dailey HA, Paw BH. Ferro chelatase forms an oligomeric complex with mitoferrin-1 and Abcb10 for erythroid heme biosynthesis. Blood 2010; 116: 628-630
  13. Park CH, Valore EV, Waring AJ, Ganz T. Hepcidin, a urinary antimicrobial peptide synthesized in the liver. J Biol Chem 2001; 276: 7806-7810
  14. Winder A, Lefkowitz R, Ghoti H, Leiba M, Ganz T, Nemeth E, Rachmilewitz EA. Urinary hepcidin excretion in patients with myelodysplastic syndrome and myelofibrosis. Br J Haematol 2008; 142: 668-680
  15. Kwapisz J, Zekanowska E, Jasiniewska J. Decreased serum prohepcidin concentration in patients with polycythemia vera. J Zhejiang Univ Sci B 2009; 10: 791-795
  16. Frazer DM,