2010 Fiscal Year Final Research Report

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

Research Project

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Project/Area Number	20591284
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Single-year Grants
Section	一般
Research Field	Pediatrics
Research Institution	Kyoto Prefectural University of Medicine
Principal Investigator	TOIYAMA Kentaro Kyoto Prefectural University of Medicine, 医学研究科, 助教 (00433285)
Co-Investigator(Kenkyū-buntansha)	KAWAI YOUKO 京都府立医科大学, 医学部・附属病院, 専攻医 (60405248) ZAWA Seiichirou 京都府立医科大学, 医学研究科, 助教 (40405246) HAMAOKA Kenji 京都府立医科大学, 医学研究科, 教授 (60189602)
Project Period (FY)	2008 – 2010
Keywords	先天性心疾患 / アポトーシス / 容量負荷 / 圧負荷 / FasL / caspase9
Research Abstract	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.