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Ann Rheum Dis:Slit2/Robo4轴导致系统性硬化症内皮细胞功能障碍和血管生成紊乱

2018-07-19 xiangting MedSci原创

从SSc疾病的超早期开始,Slit2的循环水平升高和Slit2/Robo4抗血管生成轴的激活导致外周微血管病变。

在系统性硬化症(SSc)中,早期微血管损伤之后是血管生成受损和周围毛细血管丢失。这项研究探讨了神经血管引导分子Slit2及其间接(Robo)受体对SSc相关性内皮细胞功能障碍的影响。

研究人员测定了SSc患者和健康对照的循环性Slit2水平。在SSc和健康皮肤活检和外植皮肤微血管内皮细胞(MVECs)中分析Slit2、Robo1和Robo4表达。通过细胞活力、伤口愈合和毛细血管样管形成测定来研究MVEC血管生成中的Slit2/Robo4的功能。

与对照组相比,SSc或超早期诊断为SSc(VEDOSS)患者的循环性Slit2显著升高。有趣的是,甲褶电视毛细管显微镜检查(NVC)异常的VEDOSS患者的血清Slit2水平升高,而NVC正常的VEDOSS患者和对照组相似。在SSc患者中,与对照相比,Slit2和Robo4表达在临床受影响的皮肤和外植MVECs中上调。在用重组人Slit2或SSc血清攻击后,健康MVECs的血管生成显著降低。当SSc血清与抗Slit2阻断抗体预孵育时,这些抑制作用显著减弱。在体外,SSc-MVECs的血管生成严重受损,并且可通过Slit2中和或ROBO4基因沉默得到显著改善。Slit2/Robo4轴通过抑制Src激酶磷酸化干扰血管生成。

从SSc疾病的超早期开始,Slit2的循环水平升高和Slit2/Robo4抗血管生成轴的激活导致外周微血管病变。

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    2018-07-19 1209e435m98(暂无昵称)

    学习了,谢谢分享

    0

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