Erythropoietin Receptor (EPOR) Signaling in the Osteoclast Lineage Contributes to EPO-Induced Bone Loss in Mice.
CD115
bone
erythropoietin (EPO)
erythropoietin receptor (EPOR)
osteoclasts
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
10 Oct 2022
10 Oct 2022
Historique:
received:
14
08
2022
revised:
29
09
2022
accepted:
03
10
2022
entrez:
14
10
2022
pubmed:
15
10
2022
medline:
18
10
2022
Statut:
epublish
Résumé
Erythropoietin (EPO) is a pleiotropic cytokine that classically drives erythropoiesis but can also induce bone loss by decreasing bone formation and increasing resorption. Deletion of the EPO receptor (EPOR) on osteoblasts or B cells partially mitigates the skeletal effects of EPO, thereby implicating a contribution by EPOR on other cell lineages. This study was designed to define the role of monocyte EPOR in EPO-mediated bone loss, by using two mouse lines with conditional deletion of EPOR in the monocytic lineage. Low-dose EPO attenuated the reduction in bone volume (BV/TV) in Cx3cr1
Identifiants
pubmed: 36233351
pii: ijms231912051
doi: 10.3390/ijms231912051
pmc: PMC9570419
pii:
doi:
Substances chimiques
Receptors, Erythropoietin
0
Erythropoietin
11096-26-7
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Israel Science Foundation
ID : 1188/21
Organisme : Israel Science Foundation
ID : 1086/17
Organisme : Dotan Hemato-oncology Fund, the Cancer Biology Research Center, Tel Aviv University
Organisme : German-Israeli Foundation for Scientific Research and Development
ID : I-1433-203.12/2017
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