A novel role for interferon regulatory factor 1 (IRF1) in regulation of bone metabolism

摘要: Increased risk of bone fractures is observed in patients with chronic inflammatory conditions, such as bowel disease and rheumatoid arthritis. Members the Interferon Response Factor family transcriptional regulators, IRF1 IRF8, have been identified genetic factors for several autoimmune diseases. We investigated a potential role Irf1 gene metabolism. Here, we report that Irf1−/−mutant mice show altered morphology association trabecular architecture increased cortical thickness cellularity. Ex vivo studies on cells derived from marrow stimulated Rank ligand revealed an increase size resorptive activity tartrate-resistant acid-positive Irf1−/− mutant compared wild-type control mice. deficiency was also associated decreased proliferation marrow-derived osteoblast precursors ex vivo, concomitant mineralization cells. plays metabolism suggest regulates maturation osteoclasts osteoblasts. The phenotype mutants strikingly similar to Stat1−/− mice, suggesting two interacting proteins play critical enabling common regulation these cell lineages.