| Project/Area Number |
12670486
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | OKAYAMA UNIVERSITY |
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Principal Investigator |
KOIDE Norio Okayama University, Graduate school of medicine and Dentistry, Professor, 大学院・医歯学総合研究科, 教授 (20142333)
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| Co-Investigator(Kenkyū-buntansha) |
SHINJI Toshiyuki Okayama University, University Hospital, Lecturer, 医学部付属病院, 講師 (70314680)
KUSACHI Shozo Okayama University, Medical School, Professor, 医学部, 教授 (30214943)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2002: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2001: ¥600,000 (Direct Cost: ¥600,000)
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| Keywords | extracellular-matrix remodeling / TGF-β / CTGF / liver regeneration / type I collagen / partial hepatectomy / D-galactosamine injured liver / 細胞外マトリックス |
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| Research Abstract |
Connective tissue growth factor (CTGF) is up-regulated by TGF-β1 during wound healing. Present study was to examine the expression of CTGF during regeneration after 70% partial hepatectomy (PH) or D-galactosamine (GalN) injured liver in rats. CTGF, TGF-β1, and type I collagen mRNAs were semi-quantified by a ribonuclease protection assay. After PH, TGF-β1 and type I collagen were increased at 2-6h and at 12-48h. CTGF increased at 6h, returned to the control level thereafter. Ribonuclease protection assay of cultured hepatic stellate cells (HSC) and in situ hybridization suggest that the cells express CTGF along sinusoid might be HSCs. After GalN-administration, CTGF increased at 2-96h with a shoulder peak at 6-12h followed by a main peak at 24h. TGF-β1 and type I collagen were up-regulated with kinetics similar to those of CTGF. The different kinetics between PH and GalN regenerations indicate that regulation of CTGF in the two processes is different. Higher TGF-β1 expression after infl
… More
ammatory/necrotic process in the GalN regeneration may caused the prolonged CTGF expression.
We examined the expression of CCN (Nov, CYR61 and CTGF) family genes in human hepatocellular carcinomas (HCCs) and studied the correlation of these gene expressions with clinicopathological parameters. Apair of tumor and surrounding non-tumor tissues were obtained from patients with HCC. The presence of mRNA of CCN family genes was analyzed by the reverse-transcription polymerase chain reaction. Nov, CVR61 and CTGF mRNA were identified in 17 (73.9%), 17 (73.9%), six (26.1%) tumors, and in nine (39.1%), 16 (69.6%), one (4.3%) surrounding non-tumor tissues of patients with HCC. No significant difference was found in clinicopathological parameters between cases with HCC negative and positive for these gene expressions. The prevalence of Nov and CTGF expression in HCC is significantly higher than those in surrounding non-tumor. These results suggest that Nov and CTGF is associated with the development of tumors in the liver. Less
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