[FAK-related non-kinase plasmid transfection inhibited hepatic stellate cells proliferation]

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2009 Feb;25(1):69-73.
[Article in Chinese]

Abstract

Aim: To observe the effect of FAK-related non-Kinase (FRNK) plasmid on hepatic stellate cell (HSC) proliferation stimulated by fibronectin (FN).

Methods: FRNK plasmid was transfected into HSC with transient liposomal transfection. The proteins of FRNK, FAK and p-FAK(Tyr397) were assayed by Western blotting analysis. The proliferation of HSC was evaluated by improved MTT assay, and cell cycle pattern was determined by flow cytometry (FCM).

Results: (1) The expression of FRNK protein increased after FRNK transfected HSC, and it was at 48 h that the expression of FRNK protein was the highest (P < 0.01). The protein level of FAK was no significant difference between before FRNK plasmid transfection and after transfection (P > 0.05). The expression of p-FAK(Tyr397) protein was down-regulated after FRNK had been transfected in HSC, (P < 0.01). (2) The HSC proliferation inhibition rates at 12 h, 24 h and 48 h after FRNK transfection were 20.07%, 26.16%, 29.77%, respectively (P < 0.01). (3) Compared with the non-FRNK plasmid group, the FRNK-transfected HSCs almost arrested in G0/G1 phase (71.4 +/- 2.81 vs 48.9 +/- 1.66, P < 0.01).

Conclusion: After FRNK were transfected successfully in HSCs using lipofectamine, the phosphorylation of FAK was inhibited. The HSC proliferation was restrained in a time-dependent manner and the HSC was arrested in G0/G1 phase.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line
  • Cell Proliferation*
  • Fibronectins
  • Hepatic Stellate Cells / cytology*
  • Humans
  • Phosphorylation
  • Plasmids / genetics
  • Protein-Tyrosine Kinases / genetics*
  • Transfection*

Substances

  • Fibronectins
  • FAK-related nonkinase
  • Protein-Tyrosine Kinases