Acceleration of Fracture Healing in Mouse with Deficiency of G-Protein Coupled Estrogen Receptor 1

INTRODUCTION: G Protein-coupled Estrogen Receptor 1 (GPER1) is a novel receptor that binds to estrogen with high affinity. The receptor is present on growth plate chondrocytes, osteocytes, osteoblasts, and osteoclasts and has been shown to play a functional role in promoted growth plate closure and bone remodeling [1]. The finding from a mouse study with the deficiency of GPER1 protein showed an increase of musculoskeletal growth and fat development. This suggests that GPER1 plays a significant role in bone development and remodeling [2, 4], but the role of GPER1 in bone repair and fracture healing is not clear. The purpose of this study was therefore to determine the role of GPER1 in bone healing utilizing an established mouse femur fracture model. We hypothesized that the deficiency of GPER1 enhanced bone repair by increasing bone mineral density (μCT), chondrogenesis, and biomechanical properties.