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The effect of Protease-activated-receptor family in surgical stress

Research Project

Project/Area Number 11671239
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Digestive surgery
Research InstitutionOkayama University

Principal Investigator

IWAGAKI Hiromi  Okayama University, Medical School Hospital, lecturer, 医学部・附属病院, 講師 (50240867)

Project Period (FY) 1999 – 2001
Project Status Completed (Fiscal Year 2001)
Budget Amount *help
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 2001: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 2000: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1999: ¥1,400,000 (Direct Cost: ¥1,400,000)
Keywordsprotease-activated-receptor / serine-protease / thrombin / trypsin / PAR-1 / PAR-2 / DIC / cell-growth / セリンプロテアーゼ / プロテアーゼ活性化受容体 / 外科的侵襲
Research Abstract

Human glioblastoma cell line A172 expressed protease-activated receptor-1 and -2 (PAR-1 and PAR-2). We investigated the effects of the stimulation of these receptors by receptor-activating agonist peptjdes on the Ca2+ signaling, protein kinase C translocation, cell morphology and cell proliferation in A172. Both PAR-1 agonist SFLLRN and PAR-2 agonist SLIGKV induced an increase in [Ca2+]i. The prior treatment of A172 with PAR-2 agonist SLIGKV did not influence the [Ca2+]i response to PAR-1 agonist SFLLRN or thrombin, however, the prior treatment with PAR-1 agonist SFLLRN or thrombin completely abolished the second response to PAR-2 agonist SLIGKV. Treatment with each agonist peptide produced thinner and fewer processes in A172. The PAR-2 agonist inhibited the proliferation of A172 significantly while PAR-1 agonist did not. PKC-alpha and gamma were translocated from cytosol to membrane with either PAR-1 or PAR-2 stimulation, however L was specifically translocated with SFLLRN, and lambda with SLIGKV, respectively. These results indicated that PAR-1 and PAR-2 stimulation produced a similar [Ca2+]i response and morphological changes in A172 glioblastoma while the effects on the cell proliferation and activation of PKC isozymes were distinct, suggesting that different signal transduction pathways were activated by these receptors. The unidirectional cross desensitization implies a functional linkage between PAR-1 and PAR-2 receptors.

Report

(4 results)
  • 2001 Annual Research Report   Final Research Report Summary
  • 2000 Annual Research Report
  • 1999 Annual Research Report
  • Research Products

    (4 results)

All Other

All Publications (4 results)

  • [Publications] Okamoto T, Iwagaki H. et al.: "The effects of stimulating protease-activated receptor-1 and -2 in A172 human glioblastoma"Journal of Neural Transm. 108. 125-140 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Okamoto T, Iwagaki H et al: "The effects of stimulating protease-activated receptor-1 and -2 in A172 human glioblastoma."Journal of Neural Transmission. 108 (2). 125-40 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Okamoto T, Iwagaki H, et al.: "The effects of stimulating protease-activated receptor-1 and -2 in A172 human glioblastoma"Journal of Neural Transmission. 108. 125-140 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] T.Okamoto,M.Nishibori,K.Samada,H.Iwaogaki: "The effects of stimulating protease-activated receptor-1, and-2 in Aiq2 human glioblastoma"J.Neurol Transm. (2000)

    • Related Report
      2000 Annual Research Report

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Published: 1999-04-01   Modified: 2016-04-21  

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