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A Quantitative Cell Migration Assay for Murine Enteric Neural Progenitors
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在cd39-null小鼠中出现细胞迁移和血管生成障碍.

C Goepfert1, C Sundberg, J Sévigny

  • 1Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA.

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|December 19, 2001
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核三酸二酸酶-1 (NTPDase1) /CD39对于血管形成 (血管生成) 是至关重要的. 它的缺失会影响细胞迁移和新血管生长,因为它会影响核酸信号传递.

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科学领域:

  • 血管生物学 血管生物学
  • 免疫学 免疫学 免疫学
  • 细胞信号传递 细胞信号传递

背景情况:

  • 核酸三酸二酸酶-1 (NTPDase1) /CD39是内皮细胞和单细胞上的一个关键的ectonucleotidase.
  • 它水解细胞外核酸二酸盐和三酸盐,影响血管反应.
  • 缺少CD39会破坏核酸水解,可能会通过P2受体通路影响血管生成.

研究的目的:

  • 研究NTPDase1/CD39在调节血管生成中的作用.
  • 为了确定CD39缺乏是否影响细胞透和新血管形成.

主要方法:

  • 在对照和cd39-null小鼠中的Matrigel插头血管生成的比较.
  • 在体外对单细胞/巨细胞对核酸的化学作用的评估.
  • 对P2Y受体介导的信号通路的分析.

主要成果:

  • cd39-null小鼠表现出细胞透受损,并在Matrigel插头中完全失败了新血管的生长.
  • 在cd39-null小鼠中,单细胞/巨细胞对核酸的化学反应显著降低.
  • 这种损伤与P2Y受体信号的脱敏有关.

结论:

  • 在血管生成过程中,NTPDase1/CD39在调节细胞透中起着至关重要的作用.
  • 通过NTPDase1/CD39进行细胞外核酸解对于新血管生长至关重要.