Pax5-deficient mice exhibit early onset osteopenia with increased osteoclast progenitors

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

Research output: Contribution to journalArticlepeer-review

49 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)6583-6591
Number of pages9
JournalJournal of Immunology
Volume173
Issue number11
DOIs
StatePublished - Dec 1 2004
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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