Earliest phases of chondrogenesis are dependent upon angiogenesis during ectopic bone formation in mice.

摘要: Endochondral ossification is the process where cartilage forms prior to and in which new bone during both fracture healing ectopic formation. Transitioning a highly coordinated between hypertrophic chondrocytes, vascular endothelial cells, osteoblasts osteoclasts. A critical biological that central interactions of these various cell types angiogenesis. Although it well established angiogenesis crucial for repair, less known pertaining role Furthermore, repair models are complicated by extensive trauma, subsequent inflammatory responses concurrent processes multiple tissues. In order more definitively characterize relationship postnatal endochondral ossification, model formation was used. Human demineralized matrix (DBM) implanted immune-deficient mice (rag null (B6.129S7-Rag1tm1/MOM/J)) induce bone. Inhibition with either small molecule (TNP-470) or targeted (Vascular Endothelial Growth Factor Receptor type 2 [VEGFR2] blocking antibody) prevented 83% 77%, respectively. Most striking progression chondrogenesis halted very early phases chondrocyte differentiation condensation prehypertrophy proliferative phase (VEGFR2 blockade) hypertrophy, while osteoclast recruitment resorption were almost completely inhibited. Our results demonstrate plays developmental at much earlier than suggested findings.