Mechanoreceptors in Alveolar Osteocyte

肺泡骨细胞中的机械感受器

基本信息

  • 批准号:
    07838043
  • 负责人:
  • 金额:
    $ 1.47万
  • 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:
    1995
  • 资助国家:
    日本
  • 起止时间:
    1995 至 1996
  • 项目状态:
    已结题

项目摘要

Although it is well known that bone formation is accelerated by mechanical stimuli, the signal transduction pathways involved are largely unknown. Suggested by the studies by E.Burger and others, which showed that bone cells respond to high-level and low-level stresses differently, we compared the response of newborn rat calvarial cells to mechanical stress during their development from immature osteoblasts to mature osteoblasts, further into osteocytes. We showed that the type of cells which is most sensitive to physiological stretching of less than 4,0000 mustrain is not osteoblast but young osteocyte. These cells are in transition from osteoblasts to osteocytes expressing low-level alkaline phosphatase and high-level osteocalcin. They also develop extensive cell processes which form a network of cells in bone. These young osteocytes stop proliferation in response to stretching and mineralize thir matrix. It was shown that cAMP is secreted and the expression of IGF-I and osteocalcin is induced in response to the stress.In human alveolar bone, it was not easy to clean the bone chips prior to the isolation of cells. That is probably why we could not obtain as many differentiated osteocytes as in rat calvaria. In those few successful cases, however, the response of osteocytes to the above mentioned stretching was similar to that of rat osteocytes. In other words, it was shown by RT-PCR method that osteocalcin expression was upregulated as a result of stretching. It was also suggested that amiloride sensitive channel (s) is involved in their response to stretching from our results of channel blocker studies measuringCa influx upon the exposure to lower osmotic conditions.
虽然众所周知,骨形成是由机械刺激加速,涉及的信号转导途径在很大程度上是未知的。根据E.Burger等人的研究表明,骨细胞对高水平和低水平应力的反应不同,我们比较了新生大鼠颅骨细胞从未成熟成骨细胞发育到成熟成骨细胞,再发育成骨细胞过程中对机械应力的反应。我们发现,对小于4,0000 μ应变的生理拉伸最敏感的细胞类型不是成骨细胞,而是年轻的骨细胞。这些细胞从成骨细胞向表达低水平碱性磷酸酶和高水平骨钙素的骨细胞过渡。它们还发育出广泛的细胞突起,形成骨骼中的细胞网络。这些年轻的骨细胞停止增殖以响应拉伸并矿化其基质。结果表明,在应力作用下,人牙槽骨细胞分泌cAMP,并诱导IGF-Ⅰ和骨钙素的表达。这可能是为什么我们不能获得尽可能多的分化成骨细胞在大鼠颅骨。然而,在这些少数成功的情况下,骨细胞对上述拉伸的反应与大鼠骨细胞的反应相似。也就是说,通过RT-PCR方法显示,骨钙素的表达作为牵拉的结果而上调。我们的通道阻断剂研究结果表明,在低渗透压条件下,阿米洛利敏感通道参与了对拉伸的反应。

项目成果

期刊论文数量(25)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Mikuni-Takagaki,Y.et.al.: "Extracellular processing of dentin matrix protein in mineralizing odontoblast culture." Endocrinology. 137. 2028-2035 (1996)
Mikuni-Takagaki,Y.et.al.:“矿化成牙本质细胞培养物中牙本质基质蛋白的细胞外加工。”
  • DOI:
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    0
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  • 通讯作者:
Suzuki, Y. et. al.: "Extracellular processing of bone and dentin proteins in matrix mineralization" Connect. Tissue Res.34(印刷中). (1996)
Suzuki, Y. 等人:“基质矿化中骨和牙本质蛋白的细胞外加工”Connect Tissue Res.34(出版中)。
  • DOI:
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    0
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Mikuni-Takagaki,Y.at.al.: "Extracellular processing of dentin matrix protein in mineralizing odontoblast culture." Endocrinology. 137. 2028-2035 (1996)
Mikuni-Takagaki,Y.at.al.:“矿化成牙本质细胞培养物中牙本质基质蛋白的细胞外加工。”
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    0
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  • 通讯作者:
Satoyoshi, M., Koizumi, Teranaka, T., Iwamoto, T., Takita, H., Kuboki, Y.Saito, S., Mikuni-Takagaki, Y.: "Extracellular processing of dentin matrix protein in mineralizing odonto-blast culture." Calcif.Tissue Int.57. 237-241 (1995)
Satoyoshi, M., Koizumi, Teranaka, T., Iwamoto, T., Takita, H., Kuboki, Y.Saito, S., Mikuni-Takagaki, Y.:“矿化成牙本质细胞中牙本质基质蛋白的细胞外加工
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    0
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Mikuni-Takagaki, Y.: "Matrix mincralization and the differentiation of osteocyte-like cells in culture." J. Bone Miner. Res.10. 231-242 (1995)
Mikuni-Takagaki, Y.:“基质微化和培养中骨细胞样细胞的分化。”
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TAKAGAKI Yuko其他文献

TAKAGAKI Yuko的其他文献

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{{ truncateString('TAKAGAKI Yuko', 18)}}的其他基金

Osteocyte functions in osteoporosis of underused bone. Establishing a rat underuse model and its application to the analysis of drug effect
骨细胞在未充分利用的骨质疏松症中发挥作用。
  • 批准号:
    18592075
  • 财政年份:
    2006
  • 资助金额:
    $ 1.47万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Mechanisms of fracture healing in aged mice, which is dependent on COX-2 derived PGE_2
老年小鼠骨折愈合机制,依赖于 COX-2 衍生的 PGE_2
  • 批准号:
    16592027
  • 财政年份:
    2004
  • 资助金额:
    $ 1.47万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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