晚期抗原-1 介导角膜淋巴管生成。
Very late antigen-1 mediates corneal lymphangiogenesis.
机构信息
Center for Eye Disease and Development, Program in Vision Science, University of California, Berkeley, California 94720, USA.
出版信息
Invest Ophthalmol Vis Sci. 2011 Jul 1;52(7):4808-12. doi: 10.1167/iovs.10-6580.
PURPOSE
To investigate the specific role of very late antigen-1 (VLA-1; also known as integrin α1β1) in corneal inflammatory lymphangiogenesis in vivo and lymphatic endothelial cell functions in vitro.
METHODS
A standard suture-induced corneal inflammatory lymphangiogenesis model was used in normal adult BALB/c mice to test the effect of systemic administration of VLA-1-neutralizing antibody on lymphatic formation and macrophage infiltration in vivo. Additionally, a human lymphatic endothelial cell culture system was used to examine the effect of VLA-1 gene depletion on lymphatic endothelial cell functions in vitro using small interfering RNAs.
RESULTS
These data demonstrated, for the first time, that VLA-1 blockade significantly suppressed corneal lymphangiogenesis and macrophage infiltration during inflammation. Moreover, VLA-1 gene depletion led to a marked inhibition of lymphatic endothelial cell processes of adhesion, proliferation, and capillary tube formation.
CONCLUSIONS
These novel findings together indicate that VLA-1 is critically involved in the processes of lymphangiogenesis. Further investigation on this factor may provide novel therapies for corneal inflammation, transplant rejection, and other lymphatic-related disorders in the body.
目的
研究非常晚期抗原-1（VLA-1；也称为整合素α1β1）在体内角膜炎症性淋巴管生成和体外淋巴管内皮细胞功能中的特定作用。
方法
在正常成年 BALB/c 小鼠中使用标准缝线诱导的角膜炎症性淋巴管生成模型，以测试全身性给予 VLA-1 中和抗体对体内淋巴管生成和巨噬细胞浸润的影响。此外，使用人淋巴管内皮细胞培养系统，使用小干扰 RNA 研究 VLA-1 基因耗竭对体外淋巴管内皮细胞功能的影响。
结果
这些数据首次表明，VLA-1 阻断在炎症期间显著抑制了角膜淋巴管生成和巨噬细胞浸润。此外，VLA-1 基因耗竭导致淋巴管内皮细胞的粘附、增殖和毛细血管管形成过程明显受到抑制。
结论
这些新发现共同表明 VLA-1 是淋巴管生成过程中的关键因素。对该因子的进一步研究可能为眼部炎症、移植排斥和体内其他与淋巴管相关的疾病提供新的治疗方法。
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