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小鼠钙黏蛋白-6以不依赖血小板的方式在体内介导血栓形成。

Murine cadherin-6 mediates thrombosis in vivo in a platelet-independent manner.

作者信息

Bouck Emma G, de la Fuente Maria, Zunica Elizabeth R, Li Wei, Mumaw Michele M, Nieman Marvin T

机构信息

Department of Pharmacology Case Western Reserve University Cleveland OH USA.

Deparmtent of Biomedical Sciences Marshall University Joan C. Edwards School of Medicine Huntington WV USA.

出版信息

Res Pract Thromb Haemost. 2020 Dec 4;5(1):125-131. doi: 10.1002/rth2.12458. eCollection 2021 Jan.

DOI:10.1002/rth2.12458
PMID:33537536
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7845066/
Abstract

BACKGROUND

Platelet adhesion is the critical process mediating stable thrombus formation. Previous reports of cadherin-6 on human platelets have demonstrated its role in platelet aggregation and thrombus formation.

OBJECTIVES

We aimed to further characterize the importance of cadherin-6 in thrombosis in vivo.

METHODS

Cadherin-6 platelet expression was evaluated by western blotting, flow cytometry, and immunoprecipitation. Thrombosis was evaluated using the FeCl and Rose Bengal carotid artery models in C57Bl6 mice treated with anti-cadherin-6 or IgG and wild-type or mice. Platelet function was compared in wild-type and mice using tail-clip assays, aggregometry, and flow cytometry.

RESULTS

Human platelet expression of cadherin-6 was confirmed at ~3000 copies per platelet. mice or those treated with anti-cadherin-6 antibody showed an increased time to occlusion in both thrombosis models. Cadherin-6 was not expressed on mouse platelets, and there were no differences in tail bleeding times, platelet aggregation, or platelet activation in wild-type versus mice.

CONCLUSIONS

Cadherin-6 plays an essential role in thrombosis in vivo. However, cadherin-6 is not expressed on murine platelets. These data are in contrast to human platelets, which express a functional cadherin-6/catenin complex. The essential, platelet-independent role for cadherin-6 in hemostasis may allow it to be an effective and safe therapeutic target.

摘要

背景

血小板黏附是介导稳定血栓形成的关键过程。先前关于人类血小板上钙黏蛋白-6的报道已证明其在血小板聚集和血栓形成中的作用。

目的

我们旨在进一步明确钙黏蛋白-6在体内血栓形成中的重要性。

方法

通过蛋白质免疫印迹法、流式细胞术和免疫沉淀法评估钙黏蛋白-6在血小板上的表达。在接受抗钙黏蛋白-6或免疫球蛋白G处理的C57Bl6小鼠以及野生型或基因敲除小鼠中，使用氯化铁和孟加拉玫瑰红颈动脉模型评估血栓形成情况。使用尾夹试验、血小板聚集测定法和流式细胞术比较野生型和基因敲除小鼠的血小板功能。

结果

证实人类血小板中钙黏蛋白-6的表达量约为每个血小板3000个拷贝。基因敲除小鼠或接受抗钙黏蛋白-6抗体处理的小鼠在两种血栓形成模型中均显示闭塞时间延长。小鼠血小板上不表达钙黏蛋白-6，野生型和基因敲除小鼠在尾部出血时间、血小板聚集或血小板活化方面没有差异。

结论

钙黏蛋白-6在体内血栓形成中起重要作用。然而，小鼠血小板上不表达钙黏蛋白-6。这些数据与表达功能性钙黏蛋白-6/连环蛋白复合物的人类血小板形成对比。钙黏蛋白-6在止血过程中不依赖血小板的重要作用可能使其成为一个有效且安全的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83cd/7845066/852553118660/RTH2-5-125-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83cd/7845066/4b2bcc4220d4/RTH2-5-125-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83cd/7845066/2a4f39a1e41f/RTH2-5-125-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83cd/7845066/821bd1b756e8/RTH2-5-125-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83cd/7845066/852553118660/RTH2-5-125-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83cd/7845066/4b2bcc4220d4/RTH2-5-125-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83cd/7845066/2a4f39a1e41f/RTH2-5-125-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83cd/7845066/821bd1b756e8/RTH2-5-125-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83cd/7845066/852553118660/RTH2-5-125-g004.jpg

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