Pathogenesis of intervertebral disc degeneration and functional analysis of vascular endothelial growth factor (VEGF) in the intervertebral disc

椎间盘退变的发病机制及椎间盘血管内皮生长因子(VEGF)的功能分析

基本信息

  • 批准号:
    24791570
  • 负责人:
  • 金额:
    $ 2.75万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Young Scientists (B)
  • 财政年份:
    2012
  • 资助国家:
    日本
  • 起止时间:
    2012-04-01 至 2014-03-31
  • 项目状态:
    已结题

项目摘要

The goals of this study were to examine whether Wnt signaling accelerates vascular endotherial growth factor (VEGF) expression of nucleus pulposus cells. Rat nucleus pulposus cells were cultured under normoxic or hypoxic conditions, and the expression and promoter activity of Wnt signaling and VEGF were evaluated. Nucleus pulposus cells exhibited increased beta-catenin mRNA and protein under the hypoxic condition. Nucleus pulposus cells cotransfected with the WT-beta-catenin expression plasmid or Si-beta-catenin expression, or treated with a different concentration of BIO, showed a dose-dependent increase in the activity of VEGF (V5-luc). We next measured the relative expression level of VEGF mRNA after the treatment of BIO. We analyzed protein expression with western-blot. Total beta-catenin level after the treatment of BIO increased to a greater extent in nucleus pulposus cells compared with untreated cells.
本研究的目的是检查 Wnt 信号传导是否加速髓核细胞的血管内皮生长因子 (VEGF) 表达。在常氧或低氧条件下培养大鼠髓核细胞,评估Wnt信号和VEGF的表达和启动子活性。缺氧条件下,髓核细胞表现出β-连环蛋白mRNA和蛋白质增加。共转染WT-β-连环蛋白表达质粒或Si-β-连环蛋白表达,或用不同浓度的BIO处理的髓核细胞,显示VEGF(V5-luc)活性呈剂量依赖性增加。接下来我们测量了 BIO 处理后 VEGF mRNA 的相对表达水平。我们用蛋白质印迹分析了蛋白质表达。与未处理的细胞相比,BIO处理后髓核细胞中的总β-连环蛋白水平增加了更大程度。

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
A complex interaction between Wnt signaling and TNF-α in nucleus pulposus cells.
  • DOI:
    10.1186/ar4379
  • 发表时间:
    2013-11-14
  • 期刊:
  • 影响因子:
    4.9
  • 作者:
    Hiyama A;Yokoyama K;Nukaga T;Sakai D;Mochida J
  • 通讯作者:
    Mochida J
The effects of oxygen tension and antiaging factor Klotho on the Wnt singaling in nucleus pulposus cells.
氧张力和抗衰老因子 Klotho 对髓核细胞 Wnt 信号传导的影响。
  • DOI:
  • 发表时间:
    2012
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Aini H;Ochi H;Iwata M;Okawa A;Koga D;Okazaki M;Sano A;Asou Y.;Akihiko Hiyama;Akihiko Hiyama
  • 通讯作者:
    Akihiko Hiyama
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HIYAMA Akihiko其他文献

HIYAMA Akihiko的其他文献

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{{ truncateString('HIYAMA Akihiko', 18)}}的其他基金

Analysis of transcription factors mediated by Wnt signal in intervertebral disc degeneration and search for therapeutic agents for low back pain
椎间盘退变中Wnt信号介导的转录因子分析及寻找腰痛治疗药物
  • 批准号:
    17K10945
  • 财政年份:
    2017
  • 资助金额:
    $ 2.75万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Analysis of molecular mechanism of Wnt signal and arachidonic acid cascade in intervertebral disc degeneration
Wnt信号与花生四烯酸级联在椎间盘退变中的分子机制分析
  • 批准号:
    26462252
  • 财政年份:
    2014
  • 资助金额:
    $ 2.75万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Molecular mechanisms involved in intervertebraldisc degeneration and potential new treatment strategies
椎间盘退变的分子机制和潜在的新治疗策略
  • 批准号:
    21791419
  • 财政年份:
    2009
  • 资助金额:
    $ 2.75万
  • 项目类别:
    Grant-in-Aid for Young Scientists (B)

相似海外基金

The Role of VEGF in the Development of Low Back Pain Following IVD Injury
VEGF 在 IVD 损伤后腰痛发展中的作用
  • 批准号:
    10668079
  • 财政年份:
    2023
  • 资助金额:
    $ 2.75万
  • 项目类别:
Elucidation of the mechanism of thrombin in intervertebral disc degeneration
阐明凝血酶在椎间盘退变中的作用机制
  • 批准号:
    20K17995
  • 财政年份:
    2020
  • 资助金额:
    $ 2.75万
  • 项目类别:
    Grant-in-Aid for Early-Career Scientists
Molecular biologic approach to elucidate intervertebral disc degeneration and establishment of new treatment
分子生物学方法阐明椎间盘退变并建立新的治疗方法
  • 批准号:
    20591741
  • 财政年份:
    2008
  • 资助金额:
    $ 2.75万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
椎間板変性メカニズムの解析
椎间盘退变机制分析
  • 批准号:
    18791037
  • 财政年份:
    2006
  • 资助金额:
    $ 2.75万
  • 项目类别:
    Grant-in-Aid for Young Scientists (B)
Does the collagen IX tryptophan polymorphism trigger lumbar disc degeneration?
IX胶原蛋白色氨酸多态性是否会引发腰椎间盘退变?
  • 批准号:
    16591496
  • 财政年份:
    2004
  • 资助金额:
    $ 2.75万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
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