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1999 Fiscal Year Final Research Report Summary

ROLES OF PLASMINOGEN ACTIVATORS UPON BRAIN INJURY

Research Project

Project/Area Number 10671332
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Cerebral neurosurgery
Research InstitutionKINKI UNIVERSITY

Principal Investigator

KATAOKA Kazuo  Kinki University, Dept. Neurosurgery, Associate Prof., 医学部, 助教授 (10221178)

Co-Investigator(Kenkyū-buntansha) MATSUO Osamu  Kinki University, Dept. Physiology, Prof., 医学部, 教授 (40030879)
TANEDA Mamoru  Kinki University, Dept. Neurosurgery, Prof., 医学部, 教授 (10236713)
ASAI Toshiharu  Kinki University, Dept. Neurosurgery, Associate Prof., 医学部, 講師 (20248008)
Project Period (FY) 1998 – 1999
KeywordsPlasminogen activator / Brain injury / Angiogenesis / Brain edema
Research Abstract

Urokinase type plasminogen activator (uPA) involves tissue fibrinolysis that is related to the healing process, development, and tumor invasion. Plasminogen inhibitor-1 (PAI-1) inhibits the protelytic activity of uPA and may enhance the brain vasculature after brain injury. We studied brain edema and changes in the vasculature after a brain stab wound in uPA-deficient, uPA receptor-deficient, and PAI-1-deficient mice, and control mice. Compared to control mice, the extravasation of immunoglobulin was significantly greater in PAI 1 deficient mice at 3 days after the lesion was placed, less pronounced in uPA-deficient mice and similar to the controls in uPA receptor-deficient mice. Von Willebrand factor-positive vascular structures increased in number 8 days after lesioning in PAI-1 deficient mice. Furthermore, irregular and proliferative collagen Type IV-positive microvasculatures were observed in all PAI-1-deficient mice and in 20% of control mice 8 days after lesion placement. Those findings are indicative of increased angiogenesis. Our study clearly shows that uPA contributes to the development of secondary brain damage due to a breakdown of microvascular extracellular matrix protein, and that uPA plays a role without binding to its receptor in the acute stage. PAI-1 inhibits traumatic brain edema. On the other hand, plasminogen activator facilitates angiogenesis necessary for healing after brain injury.

  • Research Products

    (8 results)

All Other

All Publications (8 results)

  • [Publications] 片岡 和夫: "能損傷後血管新生におけるPAI-1についての検討"神経外傷. 21. 63-66 (1998)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Kataoka K: "Nigral degeneration following striato-pallidal"Neurosci Lett.. 266. 220-222 (1999)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Kataoka K: "Remote Lesion in the substautia nigra caused"Acta Neurochir(Wien). 141. 669-670 (1999)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Kataoka K: "Structural fragility and inflammatory"Stroke. 30. 1396-1401 (1999)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Kataoka K, Asai T, Ueshima S, Matsuo O, Taneda M: "A study of angiogenesis after neuronal trauma in relation to plasminogen activator inhibitor-1 (Jpn)"Neurotraumatology. 21. 63-66 (1998)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Kataoka K, Asai T, Taneda M, Ueshima S, Matsuo O, Kuroda R, Carmeliet P, Collen D: "Nigral degeneration following striato-pallidal lesion in tissue type plasminogen activator deficient mice."Neurosci Lett. 266. 220-222 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Kataoka K, Asai T, Uejima T, Sakata I, Taneda M: "Remote lesion in the substrantia nigra caused by striatopallidal abscess."Acta Neurochir (Wien). 141. 669-670 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Kataoka K, Taneda M, Asai T, Kinoshita A, Ito M, Kuroda R: "Structural fragility and inflammatory response of ruptured cerebral aneurysms. A comparative study between ruptured and unruptured cerebral aneurysms."Stroke. 30. 1396-1401 (1999)

    • Description
      「研究成果報告書概要(欧文)」より

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Published: 2001-10-23  

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