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-beta 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.
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-beta 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.
Authors: A R Bauskin; H P Zhang; W D Fairlie; X Y He; P K Russell; A G Moore; D A Brown; K K Stanley; S N Breit Journal: EMBO J Date: 2000-05-15 Impact factor: 11.598
Authors: J Strelau; A Sullivan; M Böttner; P Lingor; E Falkenstein; C Suter-Crazzolara; D Galter; J Jaszai; K Krieglstein; K Unsicker Journal: J Neurosci Date: 2000-12-01 Impact factor: 6.167
Authors: A G Moore; D A Brown; W D Fairlie; A R Bauskin; P K Brown; M L Munier; P K Russell; L A Salamonsen; E M Wallace; S N Breit Journal: J Clin Endocrinol Metab Date: 2000-12 Impact factor: 5.958
Authors: Michael Dussiot; Thiago T Maciel; Aurélie Fricot; Céline Chartier; Olivier Negre; Joel Veiga; Damien Grapton; Etienne Paubelle; Emmanuel Payen; Yves Beuzard; Philippe Leboulch; Jean-Antoine Ribeil; Jean-Benoit Arlet; Francine Coté; Geneviève Courtois; Yelena Z Ginzburg; Thomas O Daniel; Rajesh Chopra; Victoria Sung; Olivier Hermine; Ivan C Moura Journal: Nat Med Date: 2014-03-23 Impact factor: 53.440
Authors: Zhaoyang Zhao; Takao Miki; Anita Van Oort-Jansen; Tomoko Matsumoto; David S Loose; Cheng Chi Lee Journal: Physiol Genomics Date: 2011-01-11 Impact factor: 3.107