Study on the expression of matrix-degrading enzymes and programmed cell death during mammalian development

哺乳动物发育过程中基质降解酶表达与程序性细胞死亡的研究

基本信息

  • 批准号:
    10670015
  • 负责人:
  • 金额:
    $ 2.05万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    1998
  • 资助国家:
    日本
  • 起止时间:
    1998 至 1999
  • 项目状态:
    已结题

项目摘要

To elucidate the significance of the PCD and machinery of the morphogenesis of palate and limb, we investigated the occurrence of the PCD and the expression of matrix-degrading enzymes in vivo using mouse fetuses and carried out a series of experiments in vitro. The results obtained are summarized as follows;1. Palatogenesis1) PCD in the midline epithelial seam is not always necessary for the mesenchymal confluence of palate shelves, 'fusion'. 2) MEE cells have an ability to autonomously differentiate into mesenchymal cells without a contact or adhesion of the opposing palatal shelves. 3) When MEE cells have fail to transform into mesenchymal cells, the MEE cells appear to undergo apoptotic cell death. 4) Matrix metalloproteinases seem to be a key molecule for not only the mesenchymal confluence, but also the terminal differentiation of MEE cells.2. Digit separation of limb bud.1) When PCD occurs in the interdigital tissues prior to digit separation, some of endothelial cells are undergo apoptosis in the regressing marginal venous sinus and interdigital microvascular plexus. 2) PCD in the interdigital tissues appears to directly contribute to the vascular remodeling, but not to digit separation. 3) The expression of gelatinize/MMP-2 mRNA is closely associated with the vascular remodeling that appears to be required for the complete separation of individual digits. 4) In hindlimbs of the Hammer-toe(Hm/Hm) mouse fetuses, the insufficient cell death between digits II and III and between digits III and IV might result in the failure not only of the separation of digits but also of regression of the interdigital microvascular plexus.In conclusion, during mammalian development, the formation of complicated structures are achieved by 'Scrap and Build' of preexisting structures resulting from the expression of matrix-degrading enzymes and the occurrence of PCD.
为了阐明PCD的意义及其在上颚和肢体形态发生中的机制,我们在小鼠胚胎中研究了PCD的发生和基质降解酶的表达,并进行了一系列体外实验。所得结果总结如下:1。1)中线上皮缝中的PCD对于腭架间质融合并不总是必需的。2) MEE细胞能够自主分化为间充质细胞,而不需要与对立的腭壁接触或粘附。3)当MEE细胞不能转化为间充质细胞时,MEE细胞出现细胞凋亡。4)基质金属蛋白酶不仅是MEE细胞间质融合的关键分子,也是MEE细胞最终分化的关键分子。肢芽趾分离。1)指间组织在分离前发生PCD时,退行边缘静脉窦和指间微血管丛内部分内皮细胞发生凋亡。2)指间组织的PCD似乎直接导致了血管重构,而不是指分离。3) gelatinize/MMP-2 mRNA的表达与血管重构密切相关,而血管重构似乎是单个手指完全分离所必需的。4)在锤趾(Hm/Hm)小鼠胎儿后肢中,指II和指III之间以及指III和指IV之间的细胞死亡不足,不仅会导致指间微血管丛的分离失败,而且会导致指间微血管丛的退化。综上所述,在哺乳动物的发育过程中,由于基质降解酶的表达和PCD的发生,复杂结构的形成是通过对原有结构的“废弃和构建”来实现的。

项目成果

期刊论文数量(10)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Takigawa,T.and Shiota,K.: "Significance of programmed cell death/apoptosis during mammalian development with special reference to palate and limb morphogenesis"Acta Histochemica et Cytochemica. 32(6). 510 (1999)
Takikawa,T. 和 Shiota,K.:“哺乳动物发育过程中程序性细胞死亡/凋亡的意义,特别是上颚和肢体形态发生”《组织化学与细胞化学学报》。
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    0
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Takigawa,T.and Shiota,K.: "Study of the differentiation of the medial edge epithelium in the developing mouse fetal palate by using a suspension single shelf culture."Acta Anatomica Nipponica. 75(1). 60 (2000)
Takikawa,T. 和 Shiota,K.:“通过使用悬浮单架培养物研究发育中的小鼠胎儿上颚内侧边缘上皮的分化。”Acta Anatomica Nipponica。
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Takigawa,T.et al.: "Study of the vascular remodelling and programmed cell death during the separation of digits in the developing mouse limb"Acta Anatomica Nipponica. 75(1). 67 (2000)
Takikawa,T.et al.:“小鼠肢体发育过程中手指分离过程中血管重塑和程序性细胞死亡的研究”Acta Anatomica Nipponica。
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Takigawa,T., et al.: "Study of the vascular remodelling and programmed cell death during the separation of digits in the developing mouse limb"Acta Anatomica Nipponica. 75(1). 67 (2000)
Takikawa,T., et al.:“小鼠肢体发育过程中手指分离过程中血管重塑和程序性细胞死亡的研究”Acta Anatomica Nipponica。
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    0
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滝川俊也、塩田浩平(分担): "臓器別アポトーシス証明法 大槻勝紀、小路武彦、渡辺慶一(編集) 第III章 C.消化器系 1.口腔とアポトーシス pp.116-117"南江堂. 259 (2000)
Toshiya Takikawa、Kohei Shiota(撰稿人):“通过器官证明细胞凋亡的方法 Katsunori Otsuki、Takehiko Koji、Keiichi Watanabe(编)第 III 章 C. 消化系统 1. 口腔和细胞凋亡 pp.116-117” Nankodo 259( 2000)
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TAKIGAWA Toshiya其他文献

TAKIGAWA Toshiya的其他文献

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{{ truncateString('TAKIGAWA Toshiya', 18)}}的其他基金

Elucidation of the mechanism to improve the cleft palate phenotype with the molecular target drug
阐明分子靶向药物改善腭裂表型的机制
  • 批准号:
    24592788
  • 财政年份:
    2012
  • 资助金额:
    $ 2.05万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Development of the preventive fetal medication of which a therapeutic target is improvement of the severity of cleft palate phenotype in the cleft palate model mouse
开发以改善腭裂模型小鼠腭裂表型严重程度为治疗目标的预防性胎儿药物
  • 批准号:
    21592349
  • 财政年份:
    2009
  • 资助金额:
    $ 2.05万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Development of new in vitro analytic systems to clarify the mechanism underlying normal palatogenesis and cleft palate formation
开发新的体外分析系统以阐明正常腭发育和腭裂形成的机制
  • 批准号:
    18590166
  • 财政年份:
    2006
  • 资助金额:
    $ 2.05万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Study on the mechanisms by which cleft palate shows its phenotypic polymorphism in mice
小鼠腭裂表型多态性机制研究
  • 批准号:
    16590144
  • 财政年份:
    2004
  • 资助金额:
    $ 2.05万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Analysis of the mechanisms of mammalian palate and limb morphogenesis
哺乳动物上颚和肢体形态发生机制分析
  • 批准号:
    12670016
  • 财政年份:
    2000
  • 资助金额:
    $ 2.05万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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