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The Korean Journal of Pathology 2003;37(2): 121-128.
Expression of TGF-beta1 and TGF-betatype II Receptor in Chemically Induced Hepatocarcinogenesis of the Rat.
Do Youn Park, Kang Woo Park, Kang Suek Suh
Department of Pathology, College of Medicine Pusan National University, Busan, Korea. mjkang@moak.chonbuk.ac.kr
BACKGROUND: Transforming growth factor (TGF)-beta1 inhibits hepatocyte proliferation by inducing apoptosis. Expression of TGF-beta1 is tightly associated with the TGF-betatype II receptor (TGR2) expression level, and has been regarded as an important change of TGF-beta1 and TGR2 during hepatocarcinogenesis. We investigated the gene expressions and protein localizations of TGF-beta1 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-beta1 and TGR2 were performed to investigate the gene expressions and protein localizations, respectively. RESULTS: The Northern blot analyses showed a slight increase of TGF-beta1 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-beta-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-beta1 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-beta.