Zinc‐Finger Transcription Factor Odd‐Skipped Related 2 Is One of the Regulators in Osteoblast Proliferation and Bone Formation

摘要: We report that Osr2 is one of the regulators osteoblast function, because dominant-negative transgenic mice exhibited decreased activity and delayed mineralization in calvarial tibial bone tissues. Our results indicate functions regulation proliferation. Introduction: Molecular mechanisms control formation have received attention with increasing knowledge related to genetic differentiation. The odd-skipped (Osr) gene a zinc-finger transcription factor recently suggested be involved formation, although little known about its role. Materials Methods: To elucidate vivo function Osr2, we generated overexpressing Osr2. Results: In this study, N-terminal–deleted was found act as mutant toward both Osr1 Osr2. Dominant-negative (Osr2ΔN) showed cortical Furthermore, soft X-ray analysis bones revealed distinctly increased radiolucency. Examinations newborn Osr2ΔN skeletons stained alcian blue alizarin red reduced intensities skull skeletal elements. Morphologically, calvariae tibias were composed markedly thinner parietal lower numbers osteoblastic cells on surfaces, indicating proliferation osteoblasts. osteoblasts obtained from highly attenuated differentiation proliferation, confirming needed for osteogenesis. Finally, Runx2-deficient cell assays induces alkaline phosphatase (ALP) expression, but lesser degree than Runx2-expressing cells. Conclusions: observations plays key role proliferation.