| First Author | Awida Z | Year | 2022 |
| Journal | Int J Mol Sci | Volume | 23 |
| Issue | 19 | PubMed ID | 36233351 |
| Mgi Jnum | J:330897 | Mgi Id | MGI:7366024 |
| Doi | 10.3390/ijms231912051 | Citation | Awida Z, et al. (2022) Erythropoietin Receptor (EPOR) Signaling in the Osteoclast Lineage Contributes to EPO-Induced Bone Loss in Mice. Int J Mol Sci 23(19) |
| abstractText | 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(Cre) EPOR(f/f) female mice (27.05%) compared to controls (39.26%), but the difference was not statistically significant. To validate these findings, we increased the EPO dose in LysM(Cre) model mice, a model more commonly used to target preosteoclasts. There was a significant reduction in both the increase in the proportion of bone marrow preosteoclasts (CD115(+)) observed following high-dose EPO administration and the resulting bone loss in LysM(Cre) EPOR(f/f) female mice (44.46% reduction in BV/TV) as compared to controls (77.28%), without interference with the erythropoietic activity. Our data suggest that EPOR in the monocytic lineage is at least partially responsible for driving the effect of EPO on bone mass. |
