2000 Fiscal Year Final Research Report Summary
REGULATION OF HEPATOCYTE GROWTH
Project/Area Number |
10470136
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Research Category |
Grant-in-Aid for Scientific Research (B).
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Gastroenterology
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Research Institution | YAMAGUCHI UNIVERSITY |
Principal Investigator |
OKITA Kiwamu YAMAGUCHI UNIVERSITY, SCHOOL OF MEDICINE, PROFESSOR, 医学部, 教授 (70107738)
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Co-Investigator(Kenkyū-buntansha) |
KUBO Yoshitugu YAMAGUCHI UNIVERSITY HOSPITAL, Clinical Fellow, 医学部・附属病院, 医員(臨床)
MASUHARA Masaaki YAMAGUCHI UNIVERSITY, SCHOOL OF MEDICINE, RESEARCH ASSOCIATE, 医学部, 助手 (80294627)
SAKAIDA Isao YAMAGUCHI UNIVERSITY HOSPITAL, RESEARCH ASSOCIATE, 医学部・附属病院, 助手 (80263763)
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Project Period (FY) |
1998 – 2000
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Keywords | HGF / TGF-β / EXTRACELLULAR MATRIX |
Research Abstract |
The reguration of hepatocyte regeneration has been thought the balane betwen inhibitory cytokines i. e. TGF-β and accelerating cytokines i. e. HGF.It has been reported that main TGF-b producing cell is the stellate cell which palys an important role of fibrosis in the liver. Under chronic inflamatory condition, either regenerated hepatocyte or extarcellular matrix, which stellate cell mainly produces, will replace the necrotic tissue. Also NK cell may be involved in the regulation of hepatocyte regeneration. The results of this study are followings ; (1) Pig serum treatment twice a week induced hepatic fibrosis with increased TGF-β expression and 70% hepatectomy of this TGF-β induced liver showed retarded regeneration compared with normal liver. (2) Choline deficient diet induced liver cirrhosis with preneoplastic lesions and hepatocellular carcinoma with incerased TGF-b expression by activated stellate cell and preneoplastic lesions are surrounded with activated stellate cell, producing TGF-β The extent of growth (regeneration) rate of these hepatocytes in the preneoplastic lesions is more than that of normal hepatocytes. Thus preneoplastic lesions are already escaped from the regulation of TGF-β. (3) NK cell may attack inmature regenerated hepatocytes and retard hepatic regeneration.
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