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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. chengyan116@126.com
  • 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.

Abstract

OBJECTIVE:

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

METHODS:

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.

RESULTS:

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).

CONCLUSION:

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.

PMID:
24386815
[PubMed - indexed for MEDLINE]
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