화학적으로 유도한 백서 간암에서 TGF-beta1 및 TGF-beta type II receptor의 발현
Expression of TGF-beta1 and TGF-beta type II Receptor in Chemically Induced Hepatocarcinogenesis of the Rat
박도윤, 박강우, 서강석,
소속 상세정보
박도윤 ( Park Do-Youn )
부산대학교 의과대학 병리학교실
박강우 ( Park Kang-Woo )
부산대학교 의과대학 병리학교실
서강석 ( Suh Kang-Suek )
부산대학교 의과대학 병리학교실
KMID : 0357920030370020121
Abstract
Background: Transforming growth factor (TGF)-beta1 inhibits hepatocyte proliferation by inducing apoptosis. Expression of TGF-beta1 is tightly associated with the TGF-beta type 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-beta1-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 reneoplastic lesions and HCC might contribute to the resistance to the growth inhibitory effects of TGF-beta1.
키워드
Carcinoma;Hepatocellular;Transforming Growth Factor beta;Blotting;Northern;Immunohistochemistry;Rats
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