Format

Send to

Choose Destination
See comment in PubMed Commons below
Arch Biochem Biophys. 2014 Nov 1;561:29-37. doi: 10.1016/j.abb.2014.06.032. Epub 2014 Jul 3.

Roles of osteoclasts in the control of medullary hematopoietic niches.

Author information

  • 1CNRS UMR7370, LP2M, Faculty of Medicine, 28 Av de Valombrose, 06107 Nice, France; University Nice Sophia Antipolis, Faculty of Sciences, Parc Valrose, 06100 Nice, France. Electronic address: blin@unice.fr.
  • 2CNRS UMR7370, LP2M, Faculty of Medicine, 28 Av de Valombrose, 06107 Nice, France; University Nice Sophia Antipolis, Faculty of Sciences, Parc Valrose, 06100 Nice, France.

Abstract

Bone marrow is the major site of hematopoiesis in mammals. The bone marrow environment plays an essential role in the regulation of hematopoietic stem and progenitor cells by providing specialized niches in which these cells are maintained. Many cell types participate to the composition and regulation of hematopoietic stem cell (HSC) niches, integrating complex signals from the bone, immune and nervous systems. Among these cells, the bone-resorbing osteoclasts (OCLs) have been described as main regulators of HSC niches. They are not limited to carving space for HSCs, but they also provide signals that affect the molecular and cellular niche components. However, their exact role in HSC niches remains unclear because of the variety of models, signals and conditions used to address the question. The present review will discuss the importance of the implication of OCLs focusing on the formation of HSC niches, the maintenance of HSCs in these niches and the mobilization of HSCs from the bone marrow. It will underline the importance of OCLs in HSC niches.

KEYWORDS:

Bone marrow; Cell mobilization; Hematopoietic niches; Osteoclasts; Osteopetrosis

PMID:
24998177
DOI:
10.1016/j.abb.2014.06.032
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center