科研之友
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摘要
Neuropeptide Y acting via it%26apos;s Y-1 receptor represents a powerful pathway in the control of bone mass. The global or osteoblast-specific Y-1 receptor deletion induces pronounced bone anabolic effects in mice. However, the contribution of Y-1 receptor deletion in bone repair/healing remained to be clarified. Therefore, in this study we characterized the role of Y-1 receptor deletion in fracture healing. Closed tibial fractures were generated in germline (Y-1(-/-)) and osteoblastic-specific Y-1 receptor knockout mice. The progression of tibial repair monitored from 1- until 6-weeks post-fracture demonstrated that in Y-1(-/-) mice there is a delay in fracture repair, as seen by a decrease in bone callus volume and callus strength. Moreover, the histological features included elevated avascular and cartilage area and consequently delayed cartilage removal, and hence impaired union. Interestingly, this delay in bone repair was not related directly to Y-1 receptors expressed by mature osteoblasts. These findings suggest that the global absence of the Y-1 receptor delays fracture healing, through impairing the early phases of fracture repair to achieve bony union. The data acquired on the role of Y-1 receptor signaling disruption in bone regeneration is critical for the design of future therapeutic strategies.
- 出版日期2013-10
- 单位河北医科大学
