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Min Xia¹, Rebekka I Stegmeyer¹, Keisuke Shirakura¹

¹Department of Vascular Cell Biology, Max Planck Institute for Molecular Biomedicine, Röntgenstr. 20, 48149, Münster, Germany.

Scientific reports

|June 24, 2024

概括

用VE-cadherin-α-catenin (VEC-αC) 基因修饰血管内皮质-cadherin (VEC) 在某些组织中阻碍白细胞扩散. 然而,中性粒细胞进入炎症腹腔的招募没有受到影响,这表明VEC-αC可以调节腹病路径.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
生理学生理学生理学

背景情况:

白血球的扩散对于免疫反应至关重要,发生在半细胞或跨细胞上.
之前的研究表明,VE-cadherin-α-catenin (VEC-αC) 融合结构块在某些组织中阻断白细胞扩散.
尽管VEC-αC表达,中性粒细胞进入炎症的腹腔的招募仍未受到影响.

研究的目的:

在VEC-αC小鼠中研究未受损的中性粒细胞在腹腔内招募的机制.
在不同的解剖部位 (cremaster肌肉和奥门) 分析中性粒细胞形路径.
确定VEC-αC在调节白细胞转移中的作用.

主要方法:

3D静脉内视频显微镜可用于可视化中性粒细胞透症.
在克雷马斯特肌肉和奥门静脉中对中性粒细胞扩散的比较.
评估内皮细胞结合完整性和粘附分子的表达 (ICAM-1,非典型的化学因子受体1).

主要成果:

中性粒细胞的扩散主要通过体中的高内皮静脉 (HEV) 发生,不受VEC-αC的影响.
在VEC-αC小鼠中,跨细胞透视显著增加,但不是在cremaster内.
与cremaster venules相比,Omental venules表现出更高的ICAM-1和非典型的化学因受体1表达以及改变的生物力学特性.
在流动下,VEC-αC表达减少了风脉内皮的延伸.

结论:

在所有静脉类型中,VE-cadherin-α-catenin (VEC-αC) 并不普遍抑制对细胞传递.
在VEC-αC融合结构可以调节中性粒细胞的路径diapedesis.
内皮细胞特性和分子表达的特定组织差异影响白细胞扩散通路.

关键词:

细胞粘附细胞粘附脑内皮质 (Endothelium) 是一个内皮质.炎症炎症是一种炎症.白血细胞的扩散.

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