IGF-I Signaling in Osterix-Expressing Cells Regulates Secondary Ossification Center Formation, Growth Plate Maturation, and Metaphyseal Formation During Postnatal Bone Development.

摘要: To investigate the role of IGF-I signaling in osterix (OSX)-expressing cells skeleton, we generated receptor (IGF-IR) knockout mice (OSXIGF-IRKO) (floxed-IGF-IR mice × OSX promoter-driven GFP-labeled cre-recombinase [OSXGFPcre]), and monitored postnatal bone development. At day 2 after birth (P2), OSXGFP-cre was highly expressed osteoblasts surface metaphysis prehypertrophic chondrocytes (PHCs) inner layer perichondral (IPCs). From P7, PHCs, IPCs, cartilage canals (CCs), (OBs) epiphyseal secondary ossification center (SOC), but only slightly OBs metaphysis. Compared with control mice, IPC proliferation decreased OSXIGF-IRKOs. In these fewer IPCs invaded into cartilage, resulting delayed formation CC SOC. Immunohistochemistry indicated a reduction vessel number lower expression VEGF ephrin B2 SOC Quantitative real-time PCR revealed that mRNA levels matrix degradation markers, MMP-9, 13 14, were OSXIGF-IRKOs compared controls. The OSXIGF-IRKO also showed irregular morphology growth plate less trabecular tibia femur from P7 to 7 weeks, accompanied by chondrocyte proliferation, altered differentiation, osteoblast differentiation. Our data indicate during development, OSX-expressing promotes increases production stimulate vascular endothelial factor (VEGF) vascularization. These processes are required for normal establishment Moreover, PHC is maturation differentiation development © 2015 American Society Bone Mineral Research.