Apoptosis and Cell Proliferation in Biliary Atresia

Research Project

Project/Area Number	09470387
Research Category	Grant-in-Aid for Scientific Research (B)
Allocation Type	Single-year Grants
Section	一般
Research Field	小児外科
Research Institution	Tohoku University
Principal Investigator	ONI Ryoji Tohoku University School of Medicine, Professor, 医学部, 教授 (50004734)
Co-Investigator(Kenkyū-buntansha)	NIO Masaki Tohoku University School of Medicine, Associate Professor, 医学部, 助教授 (70228138) SASANO Hironobu Tohoku University School of Medicine, Professor, 医学部, 教授 (50187142)
Project Period (FY)	1997 – 1998
Project Status	Completed (Fiscal Year 1998)
Budget Amount *help	¥9,700,000 (Direct Cost: ¥9,700,000) Fiscal Year 1998: ¥3,300,000 (Direct Cost: ¥3,300,000) Fiscal Year 1997: ¥6,400,000 (Direct Cost: ¥6,400,000)
Keywords	Biliary afresia / apoptosis / cell proliferation / TUNEL / ki 67 / P27 / TUNEN / 細胞回転
Research Abstract	Biliary atresia (BA), which is thought to result from progressive destruction of the bile ducts by a necroinflammatory process, is the most common cause of obstructivejaundice in infancy. Abnormalities in the tissues of remodeling ductal plates are one of the important etiologic factors but little has been studied in cell turnover of BA.Therefore, we examined programmed cell death or apoptosis by TdT-mediated dUTP biotin nick end labeling (TUNEL) and cell proliferation by Ki67 mmunostainingin in 34 cases of BA and compared the results with those of the normal control liver ( 5 cases ) and congenital dilatation of bile ducts (CDB, 5 cases) in order to study cell turnover or tissue dynamics of BA.TUNEL labeling index (LI) in bile ducts (48.913.2%) was significantly higher than that of the control normal liver (3.62.8%) and of CDB (2.55.1%). Ki67 LI in bile ducts of BA (15.05.57%) was also significantly higher than that of CDB (8.6*5.4%). No significant differences of TUNEL and Ki67 LI in hepatocytes were , however, observed among the cases with BA, CDB and normal liver. TUNEL LI was significantly higher than Ki67 LI in bile ducts of BA.BA is associated with increased and disorganized cell turnover of the bile ducts, which are related to ductal plate malformation or abnormal bile duct development.