|Budget Amount *help
¥108,290,000 (Direct Cost: ¥83,300,000、Indirect Cost: ¥24,990,000)
Fiscal Year 2009: ¥10,660,000 (Direct Cost: ¥8,200,000、Indirect Cost: ¥2,460,000)
Fiscal Year 2008: ¥21,320,000 (Direct Cost: ¥16,400,000、Indirect Cost: ¥4,920,000)
Fiscal Year 2007: ¥21,320,000 (Direct Cost: ¥16,400,000、Indirect Cost: ¥4,920,000)
Fiscal Year 2006: ¥26,650,000 (Direct Cost: ¥20,500,000、Indirect Cost: ¥6,150,000)
Fiscal Year 2005: ¥28,340,000 (Direct Cost: ¥21,800,000、Indirect Cost: ¥6,540,000)
In the present study, using the model mice associated with hypertension during pregnancy (PAH) developed in our laboratory, we have investigated (1) the pathogenesis of pregnancy-associated hypertension and the feto-maternal network, (2) the development of intrauterine growth retardation (IUGR) and its molecular mechanism, and (3) the possible involvement of a new cardiovascular system, APJ, in the pathogenesis of hypertension during pregnancy. In PAH mice, the dysfunction of endothelial cells in the placenta as the core of feto-maternal network known to play an integral part of pregnancy was observed, suggesting the development of IUGR.All pups associated with IUGR born from hypertensive mothers showed cardiac hypertrophy, anemia like phenotypes, and atrophy of many organs other than the heart, and died one day after birth. Furthermore, PAH mice showed the similar phenotypes to human HELLP syndrome. Moreover, it was suggested that APJ was involved in the exacerbation of proteinuria induced in PAH mice at the late pregnancy.