Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2014 Dec;12(4):428-32.
doi: 10.1007/s11914-014-0236-x.

Osteoblasts: a novel source of erythropoietin

Affiliations
Review

Osteoblasts: a novel source of erythropoietin

Colleen Wu et al. Curr Osteoporos Rep. 2014 Dec.

Abstract

Osteoblasts are an important cellular component of the bone microenvironment controlling bone formation and hematopoiesis. Understanding the cellular and molecular mechanisms by which osteoblasts regulate these processes is a rapidly growing area of research given the important implications for bone therapy, regenerative medicine, and hematopoietic stem cell transplantation. Here we summarize our current knowledge regarding the cellular and molecular crosstalk driving bone formation and hematopoiesis and will discuss the implications of a recent finding demonstrating that osteoblasts are a cellular source of erythropoietin .

PubMed Disclaimer

Conflict of interest statement

Conflict of Interest C. Wu, A. J. Giaccia, and E. B. Rankin declare that they have no conflicts of interest.

References

    1. Yin T, Li L. The stem cell niches in bone. J Clin Invest. 2006;116:1195–201. - PMC - PubMed
    1. Maes C, Kobayashi T, Selig MK, et al. Osteoblast precursors, but not mature osteoblasts, move into developing and fractured bones along with invading blood vessels. Dev Cell. 2010;19:329–44. - PMC - PubMed
    1. Chan CK, Chen CC, Luppen CA, et al. Endochondral ossification is required for haematopoietic stem-cell niche formation. Nature. 2009;457:490–4. - PMC - PubMed
    1. Komori T, Yagi H, Nomura S, et al. Targeted disruption of Cbfa1 results in a complete lack of bone formation owing to maturational arrest of osteoblasts. Cell. 1997;89:755–64. - PubMed
    1. Otto F, Thornell AP, Crompton T, et al. Cbfa1, a candidate gene for cleidocranial dysplasia syndrome, is essential for osteoblast differentiation and bone development. Cell. 1997;89:765–71. - PubMed

LinkOut - more resources