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Cytokine：研究发现IL-6和IL-8也参与缺氧环境下血管生成-成骨偶联过程

2018-06-24 MedSci MedSci原创

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不适当的血管生成和骨生成是骨质疏松性骨折的关键因素。缺氧是调节血管生成-成骨偶联过程的主要动力。我们最近的研究结果表明，缺氧可以通过HIF-1α通路上调VEGF促进成骨细胞的血管生成、分化和活性。本研究中，研究人员发现除了VEGF之外，在人成骨细胞MG-63、U2-OS和Saos-2细胞中，另外两种促血管生成因子IL-6和IL-8也会因缺氧和CoCl2（模拟缺氧）而上调。机制研究表明，HIF-1α

不适当的血管生成和骨生成是骨质疏松性骨折的关键因素。缺氧是调节血管生成-成骨偶联过程的主要动力。我们最近的研究结果表明，缺氧可以通过HIF-1α通路上调VEGF促进成骨细胞的血管生成、分化和活性。本研究中，研究人员发现除了VEGF之外，在人成骨细胞MG-63、U2-OS和Saos-2细胞中，另外两种促血管生成因子IL-6和IL-8也会因缺氧和CoCl2（模拟缺氧）而上调。

机制研究表明，HIF-1α（由编码有义HIF-1α的质粒转染产生）的过表达明显增加成骨细胞中IL-6和IL-8的水平。此外，使用含有IL-6或IL-8启动子序列的载体进行萤光素酶报告基因测定，以说明由HIF-1α的过表达引起的低氧诱导的IL-6和IL-8启动子活性的显著增加。此外，染色质免疫沉淀分析显示缺氧增加了HIF-1α对IL-6或IL-8启动子的DNA结合能力。通过MTT试验和Boyden小室试验的体外分析显示，外源性IL-6和IL-8可显著促进人成骨细胞、内皮细胞和单核细胞，及人内皮细胞的迁移。

总之，这些结果表明，成骨细胞中的IL-6和IL-8也可以通过HIF-1α通路促进血管生成-成骨偶联过程。除VEGF外，IL-6或IL-8靶向辅助治疗可能是改善骨质疏松症治疗的新方法。

原始出处：

Niu X, Chen Y, et al., Hypoxia regulates angeogenic-osteogenic coupling process via up-regulating IL-6 and IL-8 in human osteoblastic cells through hypoxia-inducible factor-1α pathway. Cytokine. 2018 Jun 19. pii: S1043-4666(18)30273-4. doi: 10.1016/j.cyto.2018.06.022.

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    2018-12-07 hanhaisha2020

    #研究发现#

    0

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    2018-06-26 kzlchina

    #IL-6#

    0

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    2018-06-26 zhaojie88

    #成骨#

    0

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    2018-06-26 respect

    #IL-8#

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    2018-06-24 lofter

    学习了感谢分享

    0