Inhibition of STAT1 accelerates bone fracture healing

• DOI: 10.1002/jor.21086
• Publication Date: 2010-01-08T18:07:41Z
• Authors: Kosuke Tajima; Hironari Takaishi; Jiro Takito; Takahide Tohmonda; Masaki Yoda; Norikazu Ota; Naoto Kosaki; Morio Matsumoto; Hiroyasu Ikegami; Toshiyasu Nakamura; Tokuhiro Kimura; Yasunori Okada; Keisuke Horiuchi; Kazuhiro Chiba; Yoshiaki Toyama
• Keywords: STAT1; Bone remodeling; RUNX2

Abstract Skeletal fracture healing involves a variety of cellular and molecular events; however, the mechanisms behind these processes are not fully understood. In current study, we investigated potential involvement signal transducer activator transcription 1 (STAT1), critical regulator for both osteoclastogenesis osteoblast differentiation, in skeletal healing. We used model cortical defect mice, found that callus remodeling membranous ossification highly accelerated STAT1‐deficient mice. Additionally, STAT1 suppresses Osterix transcript levels promoter activity vitro, indicating suppression as one inhibitory effect on differentiation. Furthermore, fludarabine, potent inhibitor, significantly increases bone formation heterotopic model. These results reveal previously unknown functions homeostasis may have important clinical implications treatment fracture. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:937–941,