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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 저널정보
- 대한병리학회 Journal of Pathology and Translational Medicine Journal of Pathology and Translational Medicine 제37권 제2호
- 발행연도
- 2003.1
- 수록면
- 121 - 128 (8page)
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Background : Transforming growth factor (TGF)-β1 inhibits hepatocyte proliferation by inducing apoptosis. Expression of TGF-β1 is tightly associated with the TGF-β type II receptor (TGR2) expression level, and has been regarded as an important change of TGF-β1 and
TGR2 during hepatocarcinogenesis. We investigated the gene expressions and protein localizations of TGF-β1 and TGR2 in chemical hepatocarcinogenesis. Methods : Solt and Farber’s method was used as the chemical hepatocarcinogenesis model of the rat. Northern blot analyses and immunohistochemistry for TGF-β1 and TGR2 were performed to investigate
the gene expressions and protein localizations, respectively. Results : The Northern blot analyses
showed a slight increase of TGF-β1 transcripts one month after partial hepatectomy, which is more than in sham operated control liver, and a decrease of transcripts for TGR2 two months after partial hepatectomy. The number of TGF-β1-positive preneoplastic hepatocytes was increased and correlated with the increase of the number of TGR2 negative hepatocytes or reduction of expressions of TGR2 in preneoplastic lesions. HCC tissues showed an increase of TGF-β1 protein expressions and a decrease of TGR2 compared to the adjacent liver parenchyme. Conclusion : Our data suggest that down regulation of TGR2 in preneoplastic lesions and HCC might contribute to the resistance to the growth inhibitory effects of TGF-β1.
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