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

基本信息

批准号：
20591284
负责人：
TOIYAMA Kentaro
金额：
$ 2.91万
依托单位：
Kyoto Prefectural University of Medicine
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
起止时间：
2008 至 2010
项目状态：
已结题

项目摘要

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.

已经检查了先天性心脏病的缺氧和体积超负荷大鼠模型，并检查了心肌组织的形态变化和生化变化。作为该方法，收集每个负荷结束后的心肌组织，以及1）TUNEL染料评估心肌凋亡，2）分析凋亡的信号途径，Fasl，casoase9和ask1的心脏肌肉的西部印记完成了，并完成了casoase 9的caso and ass1，ass1，ass1，ass1，ass 1内质网应激。结果是1）在TUNEL阳性中，低氧模型大鼠比假大鼠高。 2）在WesternBlot分析iCtiomysosite中，在缺氧组和体积超载组的FASL中未观察到明显的变化。但是缺氧组的caspase9和ask1较高。 3）RT-PCR的CHOP分析，缺氧组高于其他组。众所周知，内质网应力参与了缺氧负荷，并且对Ask1上游的未来信号将分析。通过使用hypoxia和体积过载心脏肌肉组织实现的DNA微阵列的基因检索，分别发现了缺氧和体积过载组的基因，并分别发现了体积过载组。