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Pax5-Deficient Mice Exhibit Early Onset Osteopenia with Increased Osteoclast Progenitors¹

Mark C. Horowitz^2,*, Yougen Xi^*, David L. Pflugh, David G. T. Hesslein, David G. Schatz^,, Joseph A. Lorenzo^¶ and Alfred L. M. Bothwell

Departments of ^* Orthopaedics and Rehabilitation and Cell Biology, Section of Immunobiology, and Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06510; and ^¶ Department of Medicine, University of Connecticut Health Center, Farmington, CT 06030

Pax5 encodes BSAP, a member of the paired box domain transcription factors, whose expression is restricted to B lymphocyte lineage cells. Pax5^–/– mice have a developmental arrest of the B cell lineage at the pro-B cell stage. We show here that Pax5^–/– mice are severely osteopenic, missing 60% of their bone mass. The osteopenia can be accounted for by a >100% increase in the number of osteoclasts in bone measured histomorphometrically. This is not due to a lack of B cells, because other strains of B cell-deficient mice do not exhibit this phenotype. There was no difference in the number of osteoclasts produced in vitro by wild-type and Pax5^–/– bone marrow cells. In contrast, spleen cells from Pax5^–/– mice produce as much as five times the number of osteoclasts as control spleen cells. Culture of Pax5^–/– spleen cells yields a population of adherent cells that grow spontaneously in culture without added growth factors for >4 wk. These cells have a monocyte phenotype, produce large numbers of osteoclasts when induced in vitro, and therefore are highly enriched in osteoclast precursors. These data demonstrate a previously unsuspected connection between B cell and osteoclast development and a key role for Pax5 in the control of osteoclast development.

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The JI 2004 173: 6499-6500. [Full Text]  

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