Basic & Clinical Medicine ›› 2007, Vol. 27 ›› Issue (2): 143-147.

• 研究论文 • Previous Articles     Next Articles

The of phosphorylated fdcal adhesion kinase in rat hepatic fibogenesis and the study on mechanism

  

  • Received:2006-06-02 Revised:2006-07-21 Online:2007-02-25 Published:2007-02-25

Abstract: Objective To observe the relationship between phosphorylation of focal adhesion kinase(FAK) and hepatic stellate cell(HSC) proliferation in fibrotic rat liver, and to study the mechanism of phosphorylated FAK regulating HSC proliferation from the cell cycle point of view. Methods The rat hepatic fibrosis was induced by bile duct ligation (BDL). Histopathological changes were evaluated by hematoxylin and eosin staining, and by Masson's trichrome method. Numbers of activated HSCs were quantified after alpha smooth muscle actin(α-SMA) staining. The proteins of p-FAK(Tyr397), Cyclin D1 and cyclin dependent kinase4 (CDK4) in the liver tissue were assayed by Western blot. Results ①With the development of hepatic fibrosis, the positive cells of α-SMA increased obviously. The positive areas of the rat livers in model groups at week 1 to 4 (12.88%±2.63%, 22.65%±2.16%, 27.45%±1.86%, 35.25%±2.34%) were larger than that in control group (5.88%±1.46%), P<0.01. ②Western blot analysis showed that in the sham-operated group, the p-FAK(Tyr397), Cyclin D1 and CDK4 was expressed a little. But with the development of liver fibrosis, the expression of the three kinds of proteins increased gradually in model groups at week 1 to 4. ③α-SMA correlated with p-FAK (Tyr397) positively, r value was 0.964, P<0.01; α-SMA correlated with Cyclin D1 and CDK4 positively, r value were 0.953 and 0.906 respectively, P<0.01; P-FAK(Tyr397) correlated with Cyclin D1 and CDK4 positively, r value were 0.969 and 0.893 respectively,P<0.01. Conclusions In hepatic fibrogenesis process, HSC became active and proliferated, while the expression of p-FAK (Tyr397), Cyclin D1 and CDK4 increased. P-FAK (Tyr397) correlated positively with Cyclin D1 and CDK4. The mechanism of phosphorylated FAK promoting hepatic fibrosis probably concerned with regulating cell cycle related protein.