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实验性牙龈炎中血管内皮生长因子受体 2 的微血管调节作用和表达增加。

Microvascular regulatory role and increased expression of vascular endothelial growth factor receptor type 2 in experimental gingivitis.

机构信息

Department of Conservative Dentistry, Faculty of Dentistry, Semmelweis University, Budapest, Hungary.

出版信息

J Periodontal Res. 2013 Apr;48(2):194-202. doi: 10.1111/j.1600-0765.2012.01520.x. Epub 2012 Sep 7.

DOI:10.1111/j.1600-0765.2012.01520.x
PMID:22957787
Abstract

OBJECTIVE

The aim of the present study was to investigate the possible microvascular regulatory role of vascular endothelial growth factor receptor type 2 (VEGFR2) in experimental gingivitis in rats.

BACKGROUND

Our previous results demonstrated that functionally active VEGFR2s are located in the venules of rat gingiva. While there is no remarkable endogenous gingival VEGF production under normal circumstances, exogenous VEGF, via VEGFR2, shows venodilatory effects. We assumed that VEGF plays an important role in vasoregulatory processes (vasodilation, increased permeability, angiogenesis) of gingival inflammation.

METHODS

Gingivitis was induced by placing ligatures and composite material around and between the lower incisors of anesthetized Wistar rats next to the gingival margin. Seven days later, VEGFR2 antagonist (ZM323881), was dripped upon the labial gingiva next to the lower incisors. Diameter changes of the selected gingival venules were measured by vital microscopy. Animals with healthy gingiva served as controls. Venule diameter changes were compared to the baseline and to control groups (no ligature). Immunohistochemical and Western blot analysis for VEGFR2 were utilized.

RESULTS

After 15, 30 and 60 min of local application of ZM323881, there was a significant venoconstriction in the inflamed gingiva compared to the baseline, while no change was recorded in controls. Endothelium, smooth muscle cells and pericytes of the gingivitis group showed increased VEGFR2 expression.

CONCLUSION

Our findings suggest that there is an increased VEGF production in gingivitis, which may play an important role in vasodilation of rat gingival venules.

摘要

目的

本研究旨在探讨血管内皮生长因子受体 2(VEGFR2)在实验性大鼠牙龈炎中的微血管调节作用。

背景

我们之前的研究结果表明,功能性活性的 VEGFR2 位于大鼠牙龈的小静脉中。虽然在正常情况下内源性牙龈 VEGF 没有明显的产生,但外源性 VEGF 通过 VEGFR2 显示出血管舒张作用。我们假设 VEGF 在牙龈炎症的血管调节过程(血管舒张、通透性增加、血管生成)中发挥重要作用。

方法

通过在下颌切牙牙龈边缘周围和之间放置结扎线和复合材料,在麻醉的 Wistar 大鼠中诱导牙龈炎。7 天后,在下颌切牙唇侧牙龈旁滴注 VEGFR2 拮抗剂(ZM323881)。通过活体显微镜测量选定的牙龈小静脉的直径变化。健康牙龈的动物作为对照。将静脉直径变化与基线和对照组(无结扎)进行比较。利用免疫组织化学和 Western blot 分析 VEGFR2。

结果

在局部应用 ZM323881 后 15、30 和 60 分钟,与基线相比,炎症性牙龈的静脉明显收缩,而对照组没有变化。牙龈炎组的内皮细胞、平滑肌细胞和周细胞显示出 VEGFR2 表达的增加。

结论

我们的研究结果表明,牙龈炎中 VEGF 的产生增加,这可能在大鼠牙龈小静脉的血管舒张中发挥重要作用。

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