The gene
phosphatase and
tensin homolog deleted on chromosome 10 (PTEN) codes for a
tumor-suppressor
phospholipid phosphatase. Deletion, mutation or abnormal expression of PTEN is commonly found in many kinds of malignant
tumors. At the time of this study, though, the role of PTEN expression in the pathology of hepatic
fibrosis remains unclear. In this study, we investigate the dynamic expression of PTEN in a rat model of hepatic
fibrosis, with special emphasis on the activation and proliferation of hepatic stellate cells (HSC) in vivo. The rat model of hepatic
fibrosis used in this study employed common bile duct
ligation. At four time points, the expression of PTEN in hepatic tissues and activated HSC in rat liver tissues was measured by immunohistochemical staining, Western blotting, real-time fluorescent quantitative PCR and immunofluorescence confocal
laser scanning microscopy, respectively. Further, alpha-smooth muscle actin (alpha-SMA), an activated HSC marker in rat liver tissues, was detected by immunohistochemical staining. This study showed that aggravation of hepatic
fibrosis led to gradually decreasing expression of PTEN in the hepatic tissues. Further, as hepatic
fibrosis worsens, PTEN-expressing activated HSC accounts for an increasingly smaller percentage of all activated HSC. In contrast, the percentage of alpha-SMA-expressing HSC cells increases significantly. In conclusion, expression of PTEN
mRNA and
protein is down-regulated in fibrogenic rat liver tissue, and its expression in HSC in vivo also decreases with progression of
fibrosis. Thus, these results show that the dynamic expression of PTEN in hepatic tissues negatively correlates with activation and proliferation of HSC.