Steatosis induced by the accumulation of apolipoprotein A-I and elevated ROS levels in H-ras12V transgenic mice contributes to hepatic lesions
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- Steatosis induced by the accumulation of apolipoprotein A-I and elevated ROS levels in H-ras12V transgenic mice contributes to hepatic lesions
- A G Wang; H B Moon; J I Chae; J M Kim; Y E Kim; Dae Yeul Yu; D S Lee
- Bibliographic Citation
- Biochemical and Biophysical Research Communications, vol. 409, no. 3, pp. 532-538
- Publication Year
- Hepatic steatosis is considered to have an important impact on liver tumorigenesis, despite a lack of clear experimental evidence. Histopathological analysis of H-ras12V transgenic mice showed liver lesions on a steatosis background had significantly higher incidence than on a non-steatosis background. Further investigation showed that apolipoprotein A-I was elevated and accumulated around fatty vacuoles. This elevated level of apolipoprotein A-I was coupled with an elevated level of H-ras12V protein and ROS. In conclusion, our results suggest that the expression of H-ras12V oncogene leads to elevated levels of ROS and apolipoprotein A-I that contribute to steatosis. The steatosis, in turn, promotes the development of hepatic lesions induced by H-ras12V oncogene.
- Apolipoprotein A-IH-ras12VHepatic lesionsSteatosisTransgenic mice
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- 1. Journal Articles > Journal Articles
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