Inhibition of STAT5A promotes osteogenesis by DLX5 regulation.

The regulation of osteogenesis is important for bone formation and fracture healing. Despite advances in understanding the molecular mechanisms of osteogenesis, crucial modulators in this process are not well-characterized. Here we demonstrate that suppression of signal transducer and activator of transcription 5A activates distal-less homeobox 5 (DLX5) in human bone marrow-derived stromal cells (hBMSCs) and enhances osteogenesis in vitro and in vivo. We show that negatively regulates expression of Dlx5 in vitro and that duanyu18135A deletion results in increased trabecular and cortical bone mass and bone mineral density in mice. Additionally, duanyu18135A deletion prevents age-related bone loss. In a murine fracture model, duanyu18135A deletion was found to significantly enhance bone remodeling by stimulating the formation of a fracture callus. Our findings indicate that duanyu18135A inhibition enhances bone formation by promoting osteogenesis of BMSCs.

KEYWORDS: {{ getKeywords(articleDetailText.words) }}