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Research for angiogenesis mechanism in hemialed disc (HD) resorption process and development of new therapies for HD using the resorption process

Research Project

Project/Area Number13671494
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Orthopaedic surgery
Research InstitutionTokyo Medical and Dental University

Principal Investigator

HARO Hirotaka  Graduated school, assistant professor, 大学院・医歯学総合研究科, 助手 (10313264)

Co-Investigator(Kenkyū-buntansha) KOMORI Hiromichi  Graduated school, associate professor, 大学院・医歯学総合研究科, 助教授 (60262169)
Project Period (FY) 2001 – 2002
Project Status Completed(Fiscal Year 2002)
Budget Amount *help
¥4,200,000 (Direct Cost : ¥4,200,000)
Fiscal Year 2002 : ¥1,100,000 (Direct Cost : ¥1,100,000)
Fiscal Year 2001 : ¥3,100,000 (Direct Cost : ¥3,100,000)
Keywordsherniated disc / spontaneous resorption / inflammatory cytokine / angiogenesis inducing factor / matrix degradation / cascade / TNF-alpha / MMPs / VEGF / sequential expressions / 血行新生 / 血管内皮細胞増殖因子(VEGF) / Matrix Metalloproteinase(MMP) / 生理的椎間板ヘルニア治療
Research Abstract

MRI analysis of herniated discs(HP)has revealed a spontaneous resorption mechanism related with neo-vascnlarization. It appears that interaction of activated macrophages with disc tissues leads to the generation of inflammnatory cytokines. Moreover, inflammatory cytokines such as tumor necrosis factor-α(TNF-α)is required for the induction of angiogenesis inducing factors such as vascular endothelial growth factor((VEGF) or matrix degrading enzymes such as MMP-3, MMP-7 and Plasmin.
We hypothesized that these molecules play a crucial role during spontaneous HD resorption. In the study we have examined the sequential expression of these molecules using a co-culture system as a model of the acute phase of disc herniation. Our results indicate that upregulation of TNF-α expression occurs first in the inflammation induced by disc herniation. VEGF upregluation follows flie increased level of TNF-α expression. Both plasmin and MMP-3 are upregulated at later time points.
Our previous work has demonstrated that TNF-α can upregulate the expression of VEGF, MMP-3 and MMP-7 under the co-culture system. Therefore, we propose that TNF-α acts as the initiator of inflammation following contact between macrophages and disc chondrocytes. TNF-α could also act to accelerate the cascade of both angiogenesis and matrix degradation thereby facilitating HD resorption. Further understanding of the resorption process may provide future novel therapies for HD.

Report

(3results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report

Research Products

(3results)

All Other

All Publications

  • [Publications] Haro Hirotaka, et al.: "Vascular Endothelial Growth Factor (VEGF) Induced Angiogenesis in Herniated Disc Resorption"Journal of Orthopaedic Research. 20. 409-415 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Haro Hirotaka, et al.: "Vascular Endothelial Growth Factor (VEGF) InducedAngiogenesis in Herniated Disc Resorption"Journal of Orthopaedic Research. 20. 409-415 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Haro Hirotaka, et al.: "Vascular Endothelial Growth Factqr (VEGF) Induced Angiogenesis in Herniated Disc Resorption"Journal of Orthopaedic Research. 20. 409-415 (2002)

    • Related Report
      2002 Annual Research Report

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Published : 2001-04-01   Modified : 2016-04-21  

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