PTH敲除小鼠体内血管形成因素对骨折愈合的影响
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国家自然科学基金(81271988)


Angiogenesis impact on fracture healing in PTH knockout mice
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    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-

    Abstract:

    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.

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周浩,孙鹏,周炜,殷国勇,凡进,李青青. PTH敲除小鼠体内血管形成因素对骨折愈合的影响[J].南京医科大学学报(自然科学版),2014,(4):462-466

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  • 收稿日期:2013-10-11
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  • 在线发布日期: 2014-04-18
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