| Co-Investigator(Kenkyū-buntansha) |
SASANO Hironobu Tohoku University, school of Medicine, Professor, 大学院・医学系研究科, 教授 (50187142)
NIO Masaki Tohoku University, school of Medicine, Associate Professor, 大学院・医学系研究科, 助教授 (70228138)
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| Budget Amount *help |
¥5,600,000 (Direct Cost: ¥5,600,000)
Fiscal Year 2002: ¥5,600,000 (Direct Cost: ¥5,600,000)
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| Research Abstract |
Biliary atresia (BA) is one of the most common causes of cholestasis leading to hepatic fibrosis in infancy. Although the etiology of BA remains largely unknown, both ductal plate malformation, immune-mediated bile duct injury and/or cell-cell adhesion, possibly associated with cell cycle and apoptosis, have been suggested to play important roles in the development of this disease. To provide a detailed insight into the genetic involvement behind the pathogenesis and disease process of BA, we evaluated the in situ gene expression profile of liver biopsy samples obtained from six infants wlth BA and two controls (normal liver and choledochal cyst) using Atlas human cDNA expression arrays (Clonetech). Among the 4,881 genes present on the array, 134 genes were found to be overe-xpressed at least 3-fold in almost all liver tissues from BA compared to corresponding controls, whereas, 25 genes were found to be down-regulated. Genes encoding cell-cell adhesion molecules, apoptotic effectors, extracellular matrices, ion transporters, immune system proteins, cytokines, growth factors, transcription factors and metabolic enzymes were differentially expressed in our study. The changes in gene expression observed in this study may be associated with the pathogenesis of BA, which may in turn contribute to secondary disease processes such as cholestasis, inflammation and fibrosis.
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