Effects of Smad4 on liver fibrosis and hepatocarcinogenesis in mice treated with CCl4/ethanol / 中华肝脏病杂志
Chinese Journal of Hepatology
; (12): 119-123, 2010.
Article
in Zh
| WPRIM
| ID: wpr-247580
Responsible library:
WPRO
ABSTRACT
To study the effects of Smad4 on liver fibrosis and hepatocarcinogenesis in mice treated with CCl(4)/ethanol. The wild-type mice (Smad4 +/+) and the Smad4 knockout mice (Smad4 +/-) were injected subcutaneously with carbon tetrachloride(CCl(4))/ethanol twice a week for twenty weeks. The expression of Smad4, TGFbeta1, Smad2, Smad3, Smad6, TIMP1, MMP2 and MMP9 was detected by RT-PCR. In the cirrhotic liver, the expression of Smad4 mRNA was significantly higher than that in the normal liver. Comparing with wild-type mice (Smad4 +/+), the TGFbeta1-Smad4 signaling was markedly attenuated in the Smad4 knockout mice (Smad4 +/-). After induction by CCl(4)/ethanol, the hepatic fibrosis in the Smad4 knockout mice (Smad4 +/-) was obviously alleviated compared with the wild-type mice (Smad4 +/+), and the incidence rate of hepatocarcinogenesis of the former was also lower than that of the latter(32.0% vs 41.9%). These results indicate that knocking out Smad4 can delay the progression of liver fibrosis and liver cancer.
Full text:
1
Index:
WPRIM
Main subject:
Pathology
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RNA, Messenger
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Carbon Tetrachloride
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Signal Transduction
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Mice, Knockout
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Tissue Inhibitor of Metalloproteinase-1
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Reverse Transcriptase Polymerase Chain Reaction
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Disease Models, Animal
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Ethanol
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Smad Proteins
Type of study:
Prognostic_studies
Limits:
Animals
Language:
Zh
Journal:
Chinese Journal of Hepatology
Year:
2010
Type:
Article