Rankl-induced osteoclastogenesis leads to loss of mineralization in a medaka osteoporosis model

摘要: Osteoclasts are macrophage-related bone resorbing cells of hematopoietic origin. Factors that regulate osteoclastogenesis great interest for investigating the pathology and treatment diseases such as osteoporosis. In mammals, receptor activator NF-κB ligand (Rankl) is a regulator osteoclast formation activation: its misexpression causes stimulation osteoporotic loss. Here, we report an phenotype induced by overexpression Rankl in medaka model. We generated transgenic lines express GFP under control cathepsin K promoter osteoclasts starting at 12 days post-fertilization (dpf), or together with CFP bi-directional heat-shock promoter. Using long-term confocal time-lapse imaging double triple larvae, monitored vivo activation osteoclasts, well their interaction osteoblasts. Upon induction, GFP-positive first observed intervertebral regions then quickly migrate to surface mineralized neural haemal arches, centra vertebral bodies. These TRAP (tartrate-resistant acid phosphatase) positive, mononuclear highly mobile dynamically extending protrusions. They exclusively found tight contact matrix. Rankl-induced resulted severe degradation matrix bodies arches. conclusion, our approach confirms conserved role teleost fish provides new insight into cellular interactions during resorption animal model useful genetic chemical screening.