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J.Health Sci., 50(3), 309-314, 2004
B-Lymphocytes are Elevated in Mouse Bone Marrow by
Estrogen Deficiency, and Induce Receptor Activator of Nuclear Factor kappa B Ligand (RANKL) Expression in Osteoblasts via Cell Adhesion
Chiho Matsumoto, Chisato Miyaura,* and Akira Ito
Department of Biochemistry, School of Pharmacy, Tokyo
University of Pharmacy and Life Science, 1432-1, Horinouchi,
Hachioji Tokyo 192-0392, Japan
Loss of estrogen caused by ovariectomy (OVX)
stimulates bone resorption and bone marrow B-lymphopoiesis, resulting in a marked bone loss and an
accumulation of B cells in mouse bone marrow. In OVX
mice, the expression of receptor activator of nuclear
factor kappa B ligand (RANKL) mRNA was elevated in
trabecular bone and bone marrow compared with sham
mice. To examine the roles of B-lymphocytes in bone
resorption, B cells were purified from bone marrow,
fixed, and co-cultured with mouse osteoblasts. Most of
the fixed B cells adhered to cell surface of osteoblasts.
The expression of RANKL mRNA in osteoblasts was markedly elevated by the contact with the fixed B cells,
and the induction rate of RANKL was correlated with
the number of B cells added. Treatment with
inhibitors of ERK 1/2 and p38 MAP kinases suppressed the
B cell-induced RANKL expression in osteoblasts,
suggesting the involvement of these kinases in the signals
via the cell-to-cell contact. These findings emphasize
the roles of B-lymphocytes in RANKL-induced osteoclastogenesis and in pathogenesis of bone loss due
to estrogen deficiency.
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