| Budget Amount *help |
¥204,360,000 (Direct Cost: ¥157,200,000、Indirect Cost: ¥47,160,000)
Fiscal Year 2016: ¥42,640,000 (Direct Cost: ¥32,800,000、Indirect Cost: ¥9,840,000)
Fiscal Year 2015: ¥41,210,000 (Direct Cost: ¥31,700,000、Indirect Cost: ¥9,510,000)
Fiscal Year 2014: ¥41,210,000 (Direct Cost: ¥31,700,000、Indirect Cost: ¥9,510,000)
Fiscal Year 2013: ¥41,600,000 (Direct Cost: ¥32,000,000、Indirect Cost: ¥9,600,000)
Fiscal Year 2012: ¥37,700,000 (Direct Cost: ¥29,000,000、Indirect Cost: ¥8,700,000)
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| Outline of Final Research Achievements |
The gallbladder excretes cytotoxic bile acids to the duodenum through the cystic duct and common bile duct system. In this study, Sox17 haploinsufficiency causes the biliary atresia-like phenotypes and hepatitis in late organogenesis mouse embryos. Transcriptomic analyses revealed the early onset of cholecystitis in the Sox17+/- embryos, together with the appearance of ectopic cystic duct-like epithelia in their gallbladders. The Sox17+/- gallbladder also showed the drastic reduction in Sonic hedgehog expression, leading to aberrant smooth muscle formation and defective contraction of the fetal gallbladder. The defective gallbladder contraction positively correlated with the severity of embryonic hepatitis in Sox17+/- embryos, suggesting the contribution of embryonic cholecystitis and fetal gallbladder contraction in the early pathogenesis of mammalian biliary atresia.
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