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[Effects of CCN5 overexpression on the expression of alpha-SMA and collagen I in hepatic stellate cells and its mechanism].

[Article in Chinese]

Author information

  • 1Shaanxi Energy Institute, Xi'an 710613, China.
  • 2Northwest University, Xi'an 710069, China.
  • 3The Fourth Hospital of Xi'an, Xi'an 710004, China.
  • 4Department of Anesthesia, Xi'an Aerospace General Hospital, Xi'an 710100, China.



To investigate the relationship between connective tissue growth factor (CCN5) and hepatic stellate cell (HSC) activation as well as the mechanism of action.


As the research object, LX-2 cells were stimulated with transforming growth factor-beta1 ( TGF-(beta1), and the protein expression levels of CCN5 and CCN2 were determined by Western blot; Hepatocyte high expression system of CCN5 was constructed and transfected hepatic stellate cells (HSC) to make CCN5 overexpression; The expression levels of alpha-smooth muscle actin (alpha-SMA) and collagen I were determined by RT-PCR and Western blot. To further study its mechanism of action, Smad2 and phosphorylation level of Smad2 were determined by RT-PCR and Western blot.


Under normal circumstances, CCN2 expression levels were much higher than CCN5 in LX-2 cells, while CCN2 expression was significantly higher than CCN5 if LX-2 cells were stimulated by TGF-beta1. However, there was no change for CCN5. Compared with the control group and the vector group, CCN5 was successfully overexpressed in the transfection group, and mRNA and protein levels of alpha-SMA and collagen I were significantly decreased (P < 0.01). Meanwhile, phosphorylation level of Smad2 was also significantly decreased (P < 0.01).


CCN5, which has the function that inhibits HSC activation, has the opposite role compared with CCN2, therefore, a new idea was proposed for the prevention and treatment of liver fibrosis.

[PubMed - indexed for MEDLINE]
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