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,¶
Departments of
*
Orthopaedic Surgery and
Cardiovascular Medicine, Faculty of Medicine, University of Tokyo, Tokyo, Japan;
Department of Biochemistry, Tokyo University of Pharmacy and Life Science, Tokyo, Japan;
Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan;
¶ Core Research for Evolutional Science and Technology, Research Development Corporation of Japan, Tokyo, Japan; and
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Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390
Osteoclasts differentiate from the hemopoietic monocyte/macrophage
cell lineage in bone marrow through cell-cell interactions between
osteoclast progenitors and stromal/osteoblastic cells. Here we show
another osteoclast differentiation pathway closely connected with B
lymphocyte differentiation. Recently the TNF family molecule osteoclast
differentiation factor/receptor activator of NF-
B ligand (ODF/RANKL)
was identified as a key membrane-associated factor regulating
osteoclast differentiation. We demonstrate that B-lymphoid lineage
cells are a major source of endogenous ODF/RANKL in bone marrow and
support osteoclast differentiation in vitro. In addition, B-lymphoid
lineage cells in earlier developmental stages may hold a potential to
differentiate into osteoclasts when stimulated with M-CSF and soluble
ODF/RANKL in vitro. B-lymphoid lineage cells may participate in
osteoclastogenesis in two ways: they 1) express ODF/RANKL to support
osteoclast differentiation, and 2) serve themselves as osteoclast
progenitors. Consistent with these observations in vitro, a decrease in
osteoclasts is associated with a decrease in B-lymphoid cells in
klotho mutant mice (KL-/-),
a mouse model for human aging that exhibits reduced turnover during
bone metabolism, rather than a decrease in the differentiation
potential of osteoclast progenitors. Taken together, B-lymphoid lineage
cells may affect the pathophysiology of bone disorders through
regulating osteoclastogenesis.
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