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Erythropoietin-driven dynamic proteome adaptations during erythropoiesis prevent iron overload in the developing embryo

Standard

Erythropoietin-driven dynamic proteome adaptations during erythropoiesis prevent iron overload in the developing embryo. / Chakraborty, Sajib; Andrieux, Geoffroy; Kastl, Philipp; Adlung, Lorenz; Altamura, Sandro; Boehm, Martin E.; Schwarzmüller, Luisa E.; Abdullah, Yomn; Wagner, Marie-Christine; Helm, Barbara; Gröne, Hermann-Josef; Lehmann, Wolf D.; Boerries, Melanie; Busch, Hauke; Muckenthaler, Martina U.; Schilling, Marcel; Klingmüller, Ursula.

In: CELL REP, Vol. 40, No. 12, 111360, 20.09.2022, p. 111360.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Chakraborty, S, Andrieux, G, Kastl, P, Adlung, L, Altamura, S, Boehm, ME, Schwarzmüller, LE, Abdullah, Y, Wagner, M-C, Helm, B, Gröne, H-J, Lehmann, WD, Boerries, M, Busch, H, Muckenthaler, MU, Schilling, M & Klingmüller, U 2022, 'Erythropoietin-driven dynamic proteome adaptations during erythropoiesis prevent iron overload in the developing embryo', CELL REP, vol. 40, no. 12, 111360, pp. 111360. https://doi.org/10.1016/j.celrep.2022.111360

APA

Chakraborty, S., Andrieux, G., Kastl, P., Adlung, L., Altamura, S., Boehm, M. E., Schwarzmüller, L. E., Abdullah, Y., Wagner, M-C., Helm, B., Gröne, H-J., Lehmann, W. D., Boerries, M., Busch, H., Muckenthaler, M. U., Schilling, M., & Klingmüller, U. (2022). Erythropoietin-driven dynamic proteome adaptations during erythropoiesis prevent iron overload in the developing embryo. CELL REP, 40(12), 111360. [111360]. https://doi.org/10.1016/j.celrep.2022.111360

Vancouver

Chakraborty S, Andrieux G, Kastl P, Adlung L, Altamura S, Boehm ME et al. Erythropoietin-driven dynamic proteome adaptations during erythropoiesis prevent iron overload in the developing embryo. CELL REP. 2022 Sep 20;40(12):111360. 111360. https://doi.org/10.1016/j.celrep.2022.111360

Bibtex

@article{65a47a287b284a34817ee5156bd8b4d4,
title = "Erythropoietin-driven dynamic proteome adaptations during erythropoiesis prevent iron overload in the developing embryo",
abstract = "Erythropoietin (Epo) ensures survival and proliferation of colony-forming unit erythroid (CFU-E) progenitor cells and their differentiation to hemoglobin-containing mature erythrocytes. A lack of Epo-induced responses causes embryonic lethality, but mechanisms regulating the dynamic communication of cellular alterations to the organismal level remain unresolved. By time-resolved transcriptomics and proteomics, we show that Epo induces in CFU-E cells a gradual transition from proliferation signature proteins to proteins indicative for differentiation, including heme-synthesis enzymes. In the absence of the Epo receptor (EpoR) in embryos, we observe a lack of hemoglobin in CFU-E cells and massive iron overload of the fetal liver pointing to a miscommunication between liver and placenta. A reduction of iron-sulfur cluster-containing proteins involved in oxidative phosphorylation in these embryos leads to a metabolic shift toward glycolysis. This link connecting erythropoiesis with the regulation of iron homeostasis and metabolic reprogramming suggests that balancing these interactions is crucial for protection from iron intoxication and for survival.",
author = "Sajib Chakraborty and Geoffroy Andrieux and Philipp Kastl and Lorenz Adlung and Sandro Altamura and Boehm, {Martin E.} and Schwarzm{\"u}ller, {Luisa E.} and Yomn Abdullah and Marie-Christine Wagner and Barbara Helm and Hermann-Josef Gr{\"o}ne and Lehmann, {Wolf D.} and Melanie Boerries and Hauke Busch and Muckenthaler, {Martina U.} and Marcel Schilling and Ursula Klingm{\"u}ller",
year = "2022",
month = sep,
day = "20",
doi = "10.1016/j.celrep.2022.111360",
language = "English",
volume = "40",
pages = "111360",
journal = "CELL REP",
issn = "2211-1247",
publisher = "Elsevier",
number = "12",

}

RIS

TY - JOUR

T1 - Erythropoietin-driven dynamic proteome adaptations during erythropoiesis prevent iron overload in the developing embryo

AU - Chakraborty, Sajib

AU - Andrieux, Geoffroy

AU - Kastl, Philipp

AU - Adlung, Lorenz

AU - Altamura, Sandro

AU - Boehm, Martin E.

AU - Schwarzmüller, Luisa E.

AU - Abdullah, Yomn

AU - Wagner, Marie-Christine

AU - Helm, Barbara

AU - Gröne, Hermann-Josef

AU - Lehmann, Wolf D.

AU - Boerries, Melanie

AU - Busch, Hauke

AU - Muckenthaler, Martina U.

AU - Schilling, Marcel

AU - Klingmüller, Ursula

PY - 2022/9/20

Y1 - 2022/9/20

N2 - Erythropoietin (Epo) ensures survival and proliferation of colony-forming unit erythroid (CFU-E) progenitor cells and their differentiation to hemoglobin-containing mature erythrocytes. A lack of Epo-induced responses causes embryonic lethality, but mechanisms regulating the dynamic communication of cellular alterations to the organismal level remain unresolved. By time-resolved transcriptomics and proteomics, we show that Epo induces in CFU-E cells a gradual transition from proliferation signature proteins to proteins indicative for differentiation, including heme-synthesis enzymes. In the absence of the Epo receptor (EpoR) in embryos, we observe a lack of hemoglobin in CFU-E cells and massive iron overload of the fetal liver pointing to a miscommunication between liver and placenta. A reduction of iron-sulfur cluster-containing proteins involved in oxidative phosphorylation in these embryos leads to a metabolic shift toward glycolysis. This link connecting erythropoiesis with the regulation of iron homeostasis and metabolic reprogramming suggests that balancing these interactions is crucial for protection from iron intoxication and for survival.

AB - Erythropoietin (Epo) ensures survival and proliferation of colony-forming unit erythroid (CFU-E) progenitor cells and their differentiation to hemoglobin-containing mature erythrocytes. A lack of Epo-induced responses causes embryonic lethality, but mechanisms regulating the dynamic communication of cellular alterations to the organismal level remain unresolved. By time-resolved transcriptomics and proteomics, we show that Epo induces in CFU-E cells a gradual transition from proliferation signature proteins to proteins indicative for differentiation, including heme-synthesis enzymes. In the absence of the Epo receptor (EpoR) in embryos, we observe a lack of hemoglobin in CFU-E cells and massive iron overload of the fetal liver pointing to a miscommunication between liver and placenta. A reduction of iron-sulfur cluster-containing proteins involved in oxidative phosphorylation in these embryos leads to a metabolic shift toward glycolysis. This link connecting erythropoiesis with the regulation of iron homeostasis and metabolic reprogramming suggests that balancing these interactions is crucial for protection from iron intoxication and for survival.

U2 - 10.1016/j.celrep.2022.111360

DO - 10.1016/j.celrep.2022.111360

M3 - SCORING: Journal article

C2 - 36130519

VL - 40

SP - 111360

JO - CELL REP

JF - CELL REP

SN - 2211-1247

IS - 12

M1 - 111360

ER -