Loss of signal transducer and activator of transcription 3 in osteoblasts impaired the bone healing in inflammatory microenvironment.

Introduction: This study aimed to investigate the effect of Stat3 on the osteoblast-mediated bone healing in the inflammatory lesion.

Methods: The conditional knockout of Stat3 in osteoblasts (Stat3 CKO) was generated via the Cre-loxP recombination system using Osterix-Cre transgenic mice. The calvarial bone inflammatory lesions were established on both Stat3 CKO and wild-type mice, then harvested to assess the bone healing.

Loss of Stat3 in Osterix cells impairs dental hard tissues development.

Background: Mutations in the signal transducers and activators of transcription 3 (STAT3) gene result in hyper-IgE syndrome(HIES), a rare immunodeficiency that causes abnormalities in immune system, bones and teeth. However, the role of Stat3 in development of dental hard tissues was yet to investigate.

Methods: In this study, a transgenic mouse of conditional knockout of Stat3 in dental mesenchymal cells (Osx-Cre; Stat3, Stat3 CKO) was made.

Loss of signal transducer and activator of transcription 3 impaired the osteogenesis of mesenchymal progenitor cells in vivo and in vitro.

Background: Signal transducer and activator of transcription 3 (Stat3) is a cytoplasmic transcription factor that participates in various biologic processes. Loss of Stat3 causes hyperimmunoglobulin E syndrome, presenting with skeletal disorders including osteoporosis, recurrent fractures, scoliosis, and craniosynostosis. The objective of this study is to explore the effect and mechanism of Stat3 on osteogenesis of mesenchymal progenitors.