Osteoblastic erythropoietin is not required for bone mass accrual

Abstract

Erythropoietin, primarily produced by interstitial fibroblasts in the kidney during adulthood, and its receptor are well-known for their crucial role in regulating erythropoiesis. Recent research has unveiled an additional function of circulating erythropoietin in the control of bone mass accrual and homeostasis through its receptor, which is expressed in both osteoblasts and osteoclasts. Notably, cells of the osteoblast lineage can produce and secrete functional erythropoietin upon activation of the hypoxia signaling pathway. However, the physiological relevance of osteoblastic erythropoietin remains to be fully elucidated. This study aimed to investigate the potential role of osteoblastic erythropoietin in regulating bone mass accrual and erythropoiesis in young adult mice. To accomplish this, we employed a mutant mouse model lacking erythropoietin specifically in mesenchymal progenitors and their descendants. Our findings indicate that in vivo loss of erythropoietin in the osteoblast lineage does not significantly affect either bone mass accrual or erythropoiesis in young adult mice. Further investigations are necessary to comprehensively understand the potential contribution of erythropoietin produced and secreted by osteoblast cells during aging, repair and under pathological conditions.