Growth differentiation factor 15 in erythroid health and disease

Toshihiko Tanno, Pierre Noel, Jeffery L. Miller

Research output: Contribution to journalReview articlepeer-review

91 Scopus citations

Abstract

PURPOSE OF REVIEW: Growth differentiation factor 15 (GDF15) was identified as a hepcidin-suppression factor that is expressed at high levels in patients with ineffective erythropoiesis. This review addresses the regulation, expression and potential functions of GDF15 in the context of erythroid biology. RECENT FINDINGS: GDF15 expression during late erythroid differentiation was discovered as part of an erythroblast transcriptome project. As GDF15 expression is associated with cellular stress or apoptosis, further investigation of the cytokine was focused upon its involvement in ineffective erythropoiesis. Remarkably high serum levels were detected in patients with thalassemia syndromes, congenital dyserythropoiesis and some acquired sideroblastic anemias. High-level GDF15 expression is not a feature of normal erythropoiesis, or erythroid recovery after bone-marrow transplantation. As GDF15 is a transforming growth factor-β superfamily member, it was investigated as an effector of ineffective erythropoiesis that suppresses hepcidin expression despite iron overloading. SUMMARY: In contrast to the low levels of GDF15 expressed during normal erythropoiesis, ineffective erythropoiesis causes high-level expression of GDF15. In patients with thalassemia and related anemias, GDF15 expression may contribute to iron overloading or other features of the disease phenotype.

Original languageEnglish (US)
Pages (from-to)184-190
Number of pages7
JournalCurrent opinion in hematology
Volume17
Issue number3
DOIs
StatePublished - May 2010

Keywords

  • GDF15
  • Ineffective erythropoiesis
  • Iron regulation

ASJC Scopus subject areas

  • Hematology

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