Studies on the Role of Aderrant Factor and Cardiac RAS for Activation of T cells in Myocardiac Infarction Transgenic Mouse

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The aim of this research project was to estabilish the transgenic mouse, which would be made by transfer renin-angiotensin system genes with cardiac specific promotor to mouse oocytes to clarify the tissue-specific role of genes of renin-angiotensin system in hte mechanism of cardiac hypertrophy. We have demonstrated that hypertrophic cardiomyopathy (HCM), especially in sporadic cases, is partially determined by genetic disposition and the molecular variant of angiotensin-converting enzyme D allele and angiotensinogen T235 seems to be a predisposing factor for cardiac hypertrophy. We have reported that in the experimental models of cardiac hypertrophy, gene expressions for renin, angiotensinogen, and angiotensin-converting enzyme were enhanced and signals leading to hypertrophy were processing through angiotensin type1 receptor and Gq coupling inositol phosphatide metabolism. We also obtained cardiac-specific promotor region of myosin to express the transfected gene within the heart. We have developed an adenovirus mediated gene transfer system, in which angiotensin-converting enzyme gene can easily transfected in vivo. Altough ther remain several steps to be overcome before making transgenic animal models of the renin-angiotensin system, these sophisticated studies provide original and important findings in the field of molecular cardiology.