• 中国科学论文统计源期刊
  • 中国科技核心期刊
  • 美国化学文摘(CA)来源期刊
  • 日本科学技术振兴机构数据库(JST)

临床输血与检验 ›› 2024, Vol. 26 ›› Issue (3): 299-308.DOI: 10.3969/j.issn.1671-2587.2024.03.002

• 基础研究 • 上一篇    下一篇

Sema7a促进内皮细胞与巨核细胞粘附的机制研究*

赖冬娣1,2, 董涵1,2, 魏亚明1,2,3, 苑召虎1,2,3   

  1. 1华南理工大学附属第二医院, 广东广州 510180;
    2广州市第一人民医院, 广东广州 510180;
    3广东省精准输血技术工程研究中心,广东广州 510180
  • 收稿日期:2024-04-15 出版日期:2024-06-20 发布日期:2024-06-24
  • 通讯作者: 魏亚明,主任技师,研究员,博士,博士生导师,主要从事输血治疗相关研究,(E-mail)eywym@scut.edu.cn。共同通信作者: 苑召虎,副主任技师,博士,硕士生导师,主要从事输血医学方面研究,(E-mail)eyyuanzhaohu@scut.edu.cn。
  • 作者简介:赖冬娣,主要从事输血医学方面研究, (E-mail)1337151807@qq.com。
  • 基金资助:
    *广东省自然科学基金省企联合项目(No. 2022A1515220019、No. 2021A1515220044)资助

Exploration of the Mechanism of Sema7a Promoting Adhesion of Umbilical Vein Endothelial Cells to Megakaryocytes

LAI Dongdi1,2, DONG Han1,2, WEI Yaming1,2,3, YUAN Zhaohu1,2,3   

  1. 1Department of Blood Transfusion, the Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong 510180;
    2Department of Blood Transfusion, Guangzhou First Peoples Hospital, Guangzhou, Guandong 510180;
    3Guangdong Engineering Research Centre of Precise Transfusion, Guangzhou,510180
  • Received:2024-04-15 Online:2024-06-20 Published:2024-06-24

摘要: 目的 本研究旨在探讨Sema7a蛋白促进内皮细胞和巨核细胞之间粘附的分子机制。方法 通过使用人脐静脉内皮细胞(human umbilical vascular endothelial cells, HUVECs)和巨核细胞系MEG01在体外模拟肺部血管和巨核细胞的粘附,使用免疫荧光、流式细胞术、4D非标记定量蛋白质组学分析等技术,检测内皮细胞与巨核细胞之间的粘附、HUVECs表面的Sema7a蛋白结合情况,及与Sema7a蛋白结合后的HUVECs蛋白质表达差异及相关生物学信息的变化,预测潜在的信号通路。并利用免疫荧光技术检测HUVECs的细胞间粘附分子1(intercellular cell adhesion molecule-1,ICAM-1)和血管黏附分子1(vascular cell adhesion molecule-1,VCAM-1)的表达。结果 Sema7a蛋白与HUVECs结合后,激活了HUVECs细胞MAPK信号通路,并上调了HVUECs的黏附分子ICAM-1和VCAM-1的表达,促进了巨核细胞MEG01与HUVECs的粘附。结论 Sema7a蛋白通过上调内皮细胞黏附分子ICAM-1和VCMA-1的表达,促进了巨核细胞MEG01与内皮细胞HUVECs间的粘附。

关键词: Sema7a, 脐静脉内皮细胞, MEG01, ICAM-1, VCAM-1

Abstract: Objective The purpose of this study was to explore the mechanism of Sema7a protein promoting the adhesion between endothelial cells and megakaryocytes. Methods Human umbilical vascular endothelial cells (HUVECs) and megakaryocyte line MEG01 were used to simulate the adhesion of pulmonary vessels and megakaryocytes in vitro. Immunofluorescence, flow cytometry, 4D Label free and other biological techniques were used to detect the adhesion between endothelial cells and megakaryocytes, the amount of Sema7a binding to HUVECs, and the changes of protein expression and biological information in HUVECs. Immunofluorescence was used to detect the expression of intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in HUVECs. Results The adhesion between MEG01 and HUVECs was promoted after Sema7a binding to HUVECs, with the MAPK signal pathway been activated, and molecules ICAM-1 and VCMA-1 of HUVECs been up-regulated. Conclusion Sema7a promoted the adhesion between megakaryocytes MEG01 and endothelial cells HUVECs by up-regulating the expression of molecules ICAM-1 and VCMA-1 in HUVECs.

Key words: Sema7a, HUVECs, MEG01, ICAM-1, VCAM-1

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