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Analysis of apoptosis signal and stem cells in congenital heart disease model rats.

Analysis of apoptosis signal and stem cells in congenital heart disease model rats.
先天性心脏病模型大鼠凋亡信号及干细胞分析
批准号:
20591284
负责人:
TOIYAMA Kentaro
金额:
$2.91万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2008
资助国家:
日本
项目状态:
已结题
起止时间:
2008 至 2010

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中文摘要
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英文摘要
A hypoxia and a volume overload rat model of congenital heart disease are made, and the morphological change of the cardiac muscle tissue and the biochemical changes have been examined. As the method, the cardiac muscle tissue after each load ended was gathered, and 1)TUNEL dye to evaluate cardiac muscle apoptosis, 2) to analyze signal pathway of apoptosis, westernblot of the cardiac muscle of FasL,casoase9, and ASK1 was done, and 3) to analyze the upstream signal of FasL, casoase9, and ASK1,RT-PCR of CHOP that is the marker of the endoplasmic reticulum stress was enforced. Result is that1) hypoxia model rats were higher in TUNEL positive than sham rats. 2) in westernblot analysis incardiomyosite, no remarkable change was observed in FasL among hypoxia group and volume overload group, sham group. But caspase9 and ASK1 were higher in hypoxia group. 3) CHOP analysis of RT-PCR, hypoxia group was higher than other groups. It was understood that the endoplasmic reticulum stress took part about a hypoxia loading, and the future signal of the upstream of ASK1 willbe analysed. The gene that was accentuated in the hypoxia and the volume overload group respectively was found though the gene retrieval by DNA microarray, that was enforced by using thehypoxia and the volume overload cardiac muscle organization to retrieve the change of the gene related to cardiac muscle apoptosis.
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会议论文
先天性心疾患動物モデル(低酸素および容量負荷)における心筋細胞apoptosisのsignal path
先天性心脏病动物模型心肌细胞凋亡信号通路(缺氧和容量超负荷)
DOI: --
发表时间: 2008
期刊:
影响因子: --
作者: [柳元孝介, 荒田道子, 櫨木大祐, 上野健太郎, 江口太助, 島子敦史, 益田君教, 野村裕一, 河野嘉文, 佐藤 恒]
通讯作者: 佐藤 恒
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