کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9252772 | 1210871 | 2005 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Hepatocyte-specific Pten-deficient mice as a novel model for nonalcoholic steatohepatitis and hepatocellular carcinoma
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کلمات کلیدی
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
بیماریهای گوارشی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Phosphatase and tensin homolog (PTEN) is a multifunctional phosphatase whose substrate is phosphatidylinositol-3,4,5-triphosphate (PIP3), and it is also a ubiquitously expressed tumor suppressor gene that down-regulates phosphatidylinositol-3-kinases (PI3Ks). Although there are a few reports about PTEN related to hepatocellular carcinoma, the role of PTEN in the liver remains unclear. Therefore, to clarify the role of PTEN in the liver, we generated and analyzed hepatocyte-specific Pten-deficient mice (Pten-deficient mice). The liver of 40-week-old Pten-deficient mice revealed macrovesicular steatosis, ballooning hepatocytes, lobular inflammatory cell infiltration, and perisinusoidal fibrosis that are characteristic of human nonalcoholic steatohepatitis (NASH). By 80 weeks of age, 100% of Pten-deficient livers showed adenomas and 66% had hepatocellular carcinomas. Thus, PTEN is important for the prevention of adipogenic and tumorigenic transformation, and Pten-deficient mice are a novel model for NASH and hepatocellular carcinoma. Our results suggest that the controlled blocking of molecules acting downstream of PI3K might provide significant therapeutic benefit to patients predisposed to NASH and hepatocellular carcinoma.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Hepatology Research - Volume 33, Issue 2, October 2005, Pages 161-166
Journal: Hepatology Research - Volume 33, Issue 2, October 2005, Pages 161-166
نویسندگان
Sumio Watanabe, Yasuo Horie, Akira Suzuki,