中国组织工程研究

中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (15): 2790-2793.doi: 10.3969/j.issn.1673-8225.2011.15.031

• 组织构建基础实验 basic experiments in tissue construction • 上一篇    下一篇

创伤后深静脉血栓形成中的黏着斑激酶信号通路

莫建文1，胡海澜2，白  波1，李  颖1，张姝江1，陈  艺1，邓晋京1   

  1. 1广州医学院第一附属医院骨科，广东省广州市  510120
    2广州医学院第二附属医院骨科，广东省广州市  510260
  • 收稿日期:2010-11-25 修回日期:2011-01-30 出版日期:2011-04-09 发布日期:2013-11-06
  • 通讯作者: 白波，教授，广州医学院第一附属医院骨科，广东省广州市 510120 drbobai@yahoo.com
  • 作者简介:莫建文☆，男，1978年生，广东省肇庆市人，汉族，2008年昆明医学院毕业，博士，主要从事创伤后深静脉血栓形成的基础与临床研究。 mjw1997@126.com
  • 基金资助:

    广东省自然科学基金面上项目(9151018201000035)，课题名称：蛋白质组学研究对创伤性深静脉血栓形成早期诊断的价值。

Influence of focal adhesion kinase signaling pathway on formation of traumatic deep vein thrombosis

Mo Jian-wen1, Hu Hai-lan2, Bai Bo1, Li Ying1, Zhang Shu-jiang1, Chen Yi1, Deng Jin-jing1   

  1. 1Department of Orthopaedics, the First Affiliated Hospital of Guangzhou Medical College, Guangzhou  510120, Guangdong Province, China
    2Department of Orthopaedics, the Second Hospital of Guangzhou Medical College, Guangzhou  510260, Guangdong Province, China
  • Received:2010-11-25 Revised:2011-01-30 Online:2011-04-09 Published:2013-11-06
  • Contact: Bai Bo, Professor, Department of Orthopaedics, the First Affiliated Hospital of Guangzhou Medical College, Guangzhou 510120, Guangdong Province, China drbobai@yahoo.com
  • About author:Mo Jian-wen☆, Doctor, Department of Orthopaedics, the First Affiliated Hospital of Guangzhou Medical College, Guangzhou 510120, Guangdong Province, China mjw1997@126.com
  • Supported by:

    the Natural Science Foundation of Guangdong Province, No. 9151018201000035*

PDF

485

被引次数

2

摘要：

背景：创伤后深静脉血栓形成的分子机制复杂，黏着斑激酶信号通路在深静脉血栓形成过程中的作用尚未阐明。
目的：探讨黏着斑激酶信号通路在创伤性深静脉血栓形成中的作用。
方法：取20只SD大鼠制备股骨骨折模型。造模后5 d，根据血栓形成情况将模型大鼠分为2组：血栓形成组和无血栓形成组，每组10只。另取10只正常大鼠作为对照组。无创切取大鼠股静脉血管组织，抽取总RNA，Genechip Rat Genome 430 2.0芯片测定股静脉RNA的表达，并分析黏着斑激酶信号通路基因表达的变化。
结果与结论：与无血栓形成组比较，血栓形成组中黏着斑激酶信号通路细胞外基质、蛋白激酶C、Fyn、辅肌动蛋白、Vav等关键基因均上调；下调的有整联蛋白α、肌球蛋白轻链磷酸酶、c-Jun基因。结果提示黏着斑激酶信号通路可能是调控血栓生物学状态的重要信号通路。

关键词: 创伤, 深静脉血栓形成, 黏着斑激酶信号通路, 基因芯片

Abstract:

BACKGROUND: The molecular mechanism of traumatic deep vein thrombosis is complex. The influence of focal adhesion kinase (FAK) signaling pathway on the development of deep vein thrombosis remains poorly understood.
OBJECTIVE: To study the effects of FAK signaling pathway in traumatic deep vein thrombosis.
METHODS: Twenty SD rats were prepared for femoral fracture models and divided into 2 groups according to thrombosis states, namely, the thrombosis and no thrombosis groups, with 10 animals in each group. Additional 10 rats served as controls. The femoral vein was incised and total RNA was extracted. The femoral vein RNA expression was detected by Genechip Rat genome 430 2.0 genechips, and the changes of FAK signaling pathway gene was analyzed. 
RESULTS AND CONCLUSION: Compared with no thrombosis group, the key genes of thrombosis group related to FAK signaling pathway of extracellular matrix, protein kinase C, Fyn, actinin and Vav were up-regulated, and integrinα, myosin light chain phosphatase and c-Jun were down-regulated. FAK signaling pathway may be one of the most important pathways to control the biological states of thrombus.

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