Vitronectin Regulates the Fibrinolytic System during the Repair of Cerebral Cortex in Stab-Wounded Mice

DOI Web Site Web Site PubMed 被引用文献3件 参考文献39件
  • Kei Hashimoto
    Graduate School of Humanities and Sciences, Ochanomizu University, Otsuka, Bunkyo-ku, Tokyo, Japan.
  • Natsumi Ikeda
    Graduate School of Humanities and Sciences, Ochanomizu University, Otsuka, Bunkyo-ku, Tokyo, Japan.
  • Mari Nakashima
    Graduate School of Humanities and Sciences, Ochanomizu University, Otsuka, Bunkyo-ku, Tokyo, Japan.
  • Hiroko Ikeshima-Kataoka
    Faculty of Science and Engineering, Waseda University, Okubo, Shinjuku-ku, Tokyo, Japan.
  • Yasunori Miyamoto
    Graduate School of Humanities and Sciences, Ochanomizu University, Otsuka, Bunkyo-ku, Tokyo, Japan.

書誌事項

公開日
2017-11-15
資源種別
journal article
権利情報
  • http://www.liebertpub.com/nv/resources-tools/text-and-data-mining-policy/121/
DOI
  • 10.1089/neu.2017.5008
公開者
SAGE Publications

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説明

Vitronectin (VN), one of the serum proteins, is known to be involved in the regulation of blood coagulation, fibrinolysis, and cell migration. It has been proposed that the regulation of fibrinolysis by VN promotes the blood-brain barrier (BBB) recovery from brain injuries such as traumatic injury and subarachnoid hemorrhage. The effects of VN on fibrinolysis in the injured brain remain unclear, however. We examined the effects of VN on the fibrinolytic system in the stab-wounded cerebral cortex of VN-knockout (KO) mice. First, hemorrhage and recovery from BBB breakdown in the wounded regions were assessed by serum immunoglobulin G (IgG) extravasation. The level of IgG extravasation increased 3-7 days after the stab wound (D3-7) in the cortex of VN-KO mice, compared with that in wild type mice, indicating that VN deficiency inhibited the recovery from BBB breakdown. The VN deficiency decreased fibrin fiber deposition at D1-3, suggesting that VN deficiency tilts the balance between fibrinogenesis and fibrinolysis toward fibrinolysis. Next, the effects of VN deficiency on the fibrinolytic factors were analyzed in the stab-wounded cortex. The VN deficiency impaired the activity of plasminogen activator inhibitor-1, an inhibitor of the fibrinolytic system, at D3-5. Further, VN deficiency up-regulated the mRNA and protein expression levels of tissue-type plasminogen activator, and urokinase-type plasminogen activator. These results demonstrate that VN contributes to the regulation of the fibrinolytic system and recovery from BBB breakdown in the wounded brain.

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