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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• 作者：Ai-Guo Wang^a ; ^{wangaiguotl@hotmail.com"" rel=""nofollow} ; Hyung-Bae Moon^b ; Jung-Il Chae^c ; Jin-Man Kim^d ; Ye-Eun Kim^f ; Dae-Yeul Yu^e ; ^{dyyu10@kribb.re.kr"" rel=""nofollow} ; Dong-Seok Lee^f ; ^g ; ^{lee1@knu.ac.kr"" rel=""nofollow}
• 关键词：Steatosis ; Apolipoprotein A-I ; Hepatic lesions ; H-ras12V ; Transgenic mice
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2011
• 出版时间：10 June 2011
• 年：2011
• 卷：409
• 期：3
• 页码：532-538
• 全文大小：841 K

文摘

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.