Epo receptor signaling in macrophages alters the splenic niche to promote erythroid differentiation.


Journal

Blood
ISSN: 1528-0020
Titre abrégé: Blood
Pays: United States
ID NLM: 7603509

Informations de publication

Date de publication:
09 07 2020
Historique:
received: 25 09 2019
accepted: 04 04 2020
pubmed: 1 5 2020
medline: 26 2 2021
entrez: 1 5 2020
Statut: ppublish

Résumé

Anemic stress induces stress erythropoiesis, which rapidly generates new erythrocytes to restore tissue oxygenation. Stress erythropoiesis is best understood in mice where it is extramedullary and occurs primarily in the spleen. However, both human and mouse stress erythropoiesis use signals and progenitor cells that are distinct from steady-state erythropoiesis. Immature stress erythroid progenitors (SEPs) are derived from short-term hematopoietic stem cells. Although the SEPs are capable of self-renewal, they are erythroid restricted. Inflammation and anemic stress induce the rapid proliferation of SEPs, but they do not differentiate until serum erythropoietin (Epo) levels increase. Here we show that rather than directly regulating SEPs, Epo promotes this transition from proliferation to differentiation by acting on macrophages in the splenic niche. During the proliferative stage, macrophages produce canonical Wnt ligands that promote proliferation and inhibit differentiation. Epo/Stat5-dependent signaling induces the production of bioactive lipid mediators in macrophages. Increased production of prostaglandin J2 (PGJ2) activates peroxisome proliferator-activated receptor γ (PPARγ)-dependent repression of Wnt expression, whereas increased production of prostaglandin E2 (PGE2) promotes the differentiation of SEPs.

Identifiants

pubmed: 32350523
pii: S0006-4971(20)61901-2
doi: 10.1182/blood.2019003480
pmc: PMC7357191
doi:

Substances chimiques

PPAR gamma 0
Pparg protein, mouse 0
Receptors, Erythropoietin 0
STAT5 Transcription Factor 0
9-deoxy-delta-9-prostaglandin D2 60203-57-8
Dinoprostone K7Q1JQR04M
Prostaglandin D2 RXY07S6CZ2

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

235-246

Subventions

Organisme : NIDDK NIH HHS
ID : R01 DK077152
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK080040
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK119865
Pays : United States

Informations de copyright

© 2020 by The American Society of Hematology.

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Auteurs

Yuanting Chen (Y)

Graduate Program in Molecular, Cellular, and Integrative Biosciences, Huck Institutes of the Life Sciences.

Jie Xiang (J)

Graduate Program in Molecular, Cellular, and Integrative Biosciences, Huck Institutes of the Life Sciences.

Fenghua Qian (F)

Graduate Program in Pathobiology.

Bastihalli T Diwakar (BT)

Department of Veterinary and Biomedical Sciences, and.

Baiye Ruan (B)

Graduate Program in Pathobiology.

Siyang Hao (S)

Graduate Program in Molecular, Cellular, and Integrative Biosciences, Huck Institutes of the Life Sciences.

K Sandeep Prabhu (KS)

Graduate Program in Molecular, Cellular, and Integrative Biosciences, Huck Institutes of the Life Sciences.
Graduate Program in Pathobiology.
Department of Veterinary and Biomedical Sciences, and.
Center for Molecular Immunology and Infectious Disease, The Pennsylvania State University, University Park, PA.

Robert F Paulson (RF)

Graduate Program in Molecular, Cellular, and Integrative Biosciences, Huck Institutes of the Life Sciences.
Graduate Program in Pathobiology.
Department of Veterinary and Biomedical Sciences, and.
Center for Molecular Immunology and Infectious Disease, The Pennsylvania State University, University Park, PA.

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Classifications MeSH