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Chinese Journal of Hepatic Surgery(Electronic Edition) ›› 2014, Vol. 03 ›› Issue (03): 178-182. doi: 10.3877/cma.j.issn.2095-3232.2014.03.012

Special Issue:

• Basic Researches • Previous Articles     Next Articles

Regulatory mechanism of activated hepatic stellate cell in the microvascular generation of hepatocellular carcinoma

Yanzhu Li1, Nan Lin1, Yi Lu1, Bing Zhu1, Ruiyun Xu1,()   

  1. 1. Department of Hepatobiliary Surgery, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China
  • Received:2014-03-07 Online:2014-06-10 Published:2014-06-10
  • Contact: Ruiyun Xu
  • About author:
    Corresponding author: Xu Ruiyun, Email:

Abstract:

Objective

To investigate the regulatory mechanism of activated hepatic stellate cell (aHSC) in the microvascular generation of hepatocellular carcinoma (HCC).

Methods

Tissue samples of 25 patients with HCC who underwent liver resection in Department of Hepatobiliary Surgery, the Third Affiliated Hospital of Sun Yat-sen University from January to December 2013 were collected. The informed consents of all patients were obtained and the ethical committee approval was received. There were 21 males and 4 females with age ranging from 29 to 75 years old and the median age of 54 years old. The HCC tissues (HCC group) and peri-cancer tissues (peri-cancer group) were collected and normal liver tissues of 21 cases were collected as control group. The expressions of smooth muscle actin (SMA), angiogenin (Ang-1), and cluster of differentiation (CD) 34 were detected by immunohistochemistry. The expression level of Ang-1 was detected by Western blot. The high expression of SMA in HCC tissues was regarded as a marker of aHSC. The differences of 3 groups were compared using one-way analysis of variance and LSD-t test. Spearman correlation analysis was used to analyze the correlations between different proteins expression.

Results

The mean of optical densities of SMA in HCC, peri-cancer, control group were (4.56±0.64)×104, (2.71±0.37)×104, (2.25±0.48)×104 respectively, which was significantly higher in HCC group than those in peri-cancer group and control group (LSD-t=7.09, 7.42; P<0.05). The optical densities of Ang-1 in 3 groups were (3.11±0.27)×105, (2.28±0.20)×105, (1.26±0.15)×105 respectively, which was significantly higher in HCC group than those in peri-cancer group and control group (LSD-t=3.00, 3.14; P<0.05). The relative gray values of Ang-1 expression in 3 groups were 4.33±1.17, 1.62±0.33, 1.60±0.38 respectively, which was significantly higher in HCC group than those in peri-cancer group and control group (LSD-t=2.71, 2.74; P<0.05). The optical intensities of CD34 in 3 groups were (18.3±0.36)×103, (5.75±1.17)×103, (2.75±0.72)×103 respectively, which was significantly higher in HCC group than those in peri-cancer group and control group (LSD-t=3.21, 3.36; P<0.05). There were positive correlations between SMA, Ang-1, CD34 (r=0.442, 0.449, 0.582; P<0.05).

Conclusions

High expressions of SMA, Ang-1 and CD34 can be observed in HCC group and closely related with each other. SMA marked aHSC can be observed in the HCC tissues. The aHSC may promote the microvascular generation of HCC by secreting Ang-1.

Key words: Carcinoma, hepatocellular, Angiopoietin-1, Microvessels, Hepatic stellate cell

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