中国组织工程研究

中国组织工程研究 ›› 2012, Vol. 16 ›› Issue (24): 4417-4421.doi: 10.3969/j.issn.1673-8225.2012.24.010

• 血管组织构建 vascular tissue construction • 上一篇    下一篇

血管组织中Plaur和Plat诱导血管性血友病因子释放促血栓形成

胡继红1，吴雪梅2，李宏昆2，李兴国2，周如丹2，赵学凌2，王 兵2   

  1. 昆明医学院第一附属医院，1放射科，2骨科，云南省昆明市 50032
  • 收稿日期:2012-03-09 修回日期:2012-04-20 出版日期:2012-06-10 发布日期:2013-11-05
  • 通讯作者: 赵学凌，博士，主任医师，昆明医学院第一附属医院骨科，云南省昆明市650032 akenika@hotmail.com
  • 作者简介:胡继红★，男，1967年生，云南省昆明市人，汉族，1993年昆明医学院毕业，硕士，副教授，主要从事深静脉血栓的基础及临床研究。 67420hjh@sohu.com
  • 基金资助:

    国家自然科学基金资助项目(30960389，81060151)；云南省科技厅-昆明医学院联合项目(2009cd159)

Plaur and Plat in vascular tissues induce von Willebrand factor release to promote deep venous thrombosis

Hu Ji-hong1, Wu Xue-mei2, Li Hong-kun2, Li Xing-guo2, Zhou Ru-dan2, Zhao Xue-ling2, Wang Bing2   

  1. 1Department of Radiology, 2Department of Orthopedics, First Affiliated Hospital of Kunming Medical College, Kunming 650032, Yunnan Province, China
  • Received:2012-03-09 Revised:2012-04-20 Online:2012-06-10 Published:2013-11-05
  • Contact: Zhao Xue-ling, Doctor, Chief physician, Department of Orthopedics, First Affiliated Hospital of Kunming Medical College, Kunming 650032, Yunnan Province, China akenika@hotmail.com
  • About author:Hu Ji-hong★, Master, Associate professor, Department of Radiology, First Affiliated Hospital of Kunming Medical College, Kunming 650032, Yunnan Province, China 67420hjh@sohu.com

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被引次数

1

摘要：

背景：目前，深静脉血栓形成的分子病因学机制及其形成的核心调控网络仍未完全阐明，对于深静脉血栓的早期诊断预测也无理想的方法。
目的：观察创伤性深静脉血栓形成大鼠静脉内皮细胞中Plaur和Plat的促血栓形成作用。
方法：采用股静脉钳夹联合下肢石膏制动构建大鼠创伤性深静脉血栓模型。依据取材时间及是否有血栓形成分为血栓形成前组、血栓形成组和血栓不形成组，分别于造模后2.5，25 h取大鼠股静脉内皮细胞用于实验。
结果与结论：基因芯片分析及real-time PCR结果均显示创伤后2.5 h，大鼠股静脉Plaur、Plau及血管性血友病因子基因表达上调；血栓形成时，Plaur、Plau及血管性血友病因子基因表达上调更显著。信号通路分析显示Plaur、Plau为血管性血友病因子的上游调控基因，血管性血友病因子为触发血小板黏附、聚集及血栓形成的关键基因。提示Plaur、Plau可通过上调血管性血友病因子表达，引发血小板黏附、聚集，促进大鼠创伤性深静脉血栓形成。

关键词: 深静脉血栓, Plat, Plaur, 血管性血友病因子, 信号通路, 内皮细胞

Abstract:

BACKGROUND: At present, the core control network, molecular etiology and mechanism of deep vein thrombosis is still not completely clear, furthermore, there is no ideal method for early diagnosis of deep venous thrombosis.
OBJECTIVE: To observe the prothrombotic role of Plaur and Plat in the vein endothelial cells in rats with traumatic deep vein thrombosis.
METHODS: Clamps plus lower limb immobilization with plaster spica were used to establish rat traumatic deep vein thrombosis models. Based on time points and whether thrombosis occurred, the experiment animals were divided into pre-thrombosis, thrombosis, and non-thrombosis groups, and then femoral vein endothelial cells were harvested at 2.5 and 25 hours after modeling.
RESULTS AND CONCLUSION: Gene chip analysis and real-time PCR results showed that after trauma 2.5 hours, mRNA expressions of Plaur, Plau and von Willebrand factor in the femoral vein were raised. In the process of thrombosis, Plaur, Plau and Von Willebrand factor mRNA expressions were significantly increased. Signal path analysis showed that the Plaur and Plau were upstream regulation genes for von Willebrand factor, and von Willebrand factor was the key gene for triggering platelet adhesion, aggregation and thrombosis. These findings imply that Plaur and Plau can be raised by up-regulation of von Willebrand factor expression, further to cause platelet adhesion and aggregation, and to promote traumatic deep vein thrombosis in rats.

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