PTH敲除小鼠体内血管形成因素对骨折愈合的影响  

Angiogenesis impact on fracture healing in PTH knockout mice

作　　者：周浩[1] 孙鹏[1] 周炜[1] 殷国勇[1] 凡进[1] 李青青[1] 

机构地区：[1]南京医科大学第一附属医院骨科,江苏南京210029

出　　处：《南京医科大学学报（自然科学版）》2014年第4期462-466,共5页Journal of Nanjing Medical University(Natural Sciences)

基　　金：国家自然科学基金(81271988)

摘　　要：目的:探究内源性甲状旁腺激素(parathyroid hormone,PTH)缺失是否通过降低血管内皮生长因子(vascular endothelial growth factor,VEGF)的表达,导致骨折愈合过程中血管再生减弱,延迟骨折愈合。方法:构建PTH基因敲除(PTHKO)小鼠的骨折模型,摄X线片观察骨折愈合情况,用免疫组化方式检测骨合成代谢以及血管形成指标。结果:PTHKO小鼠VEGF表达量下降,血小板内皮细胞黏附分子(platelet endothelial cell adhension molecule,PEGAM)免疫组化阳性减少,骨钙蛋白(osteocalcin,OCN)活性下降,骨折愈合延迟。结论:内源性PTH缺失可能通过减少间充质干细胞或成骨细胞释放VEGF,导致骨折端血管减少,成骨活性受到抑制,从而影响软骨内成骨,最终导致骨折愈合延迟。Objective：To explore whether the lack of endogenous PTH causes angiogenesis weakness by reducing the expression of VEGF during fracture healing and delays fracture healing. Methods：We constructed PTH knockouted mice fracture model,and observed fracture healing from X-ray film and detected bone anabolism and angiogenesis using immunohistochemistry. Results：VEGF expression was decreased in PTHKO mice. Immunohistochemical analysis showed that positive PEGAM was reduced. OCN activity was decreased and fracture healing was delayd. Conclusion：Lack of endogenous PTH may release VEGF by reducing mesenchymal stem cells or osteoblasts,reduce vascular fracture,inhibit osteoblastic activity, surpress endochondral ossification and lead to fracture healing delay eventually.

关 键 词：PTH VEGF 血管形成 骨折愈合 

分 类 号：R683[医药卫生—骨科学]