Objective: The mechanisms responsible for increased collagen production and hepatic fibrosis in biliary atresia (BA) remain largely unknown. We evaluated α-smooth muscle actin (α-SMA) expression in liver and the porta hepatis in infants with BA.
Methods: Immunohistochemical staining for α-SMA and CD68 in the BA liver and porta hepatis was performed. A semiquantitative 3-grade staging system was employed to estimate liver fibrosis. The densities of CD68 in BA liver and the levels of direct bilirubin were assessed in relation to α-SMA expression.
Results: α-SMA was found to be overexpressed in epithelial cells and in periductular collagen fibers. The expression in infants with BA was higher than that in the control group (P < 0.05). The amount of α-SMA in BA was positively correlated with liver fibrosis scores (r = 0.549, P = 0.022). The levels of α-SMA in the liver of BA were negatively related with improvements in direct bilirubin levels, 3 months postoperatively (r = −0.653, P = 0.029). The correlation between the α-SMA and CD-68 expression was not significantly different (r = 0.444, P = 0.057).
Conclusions: The expression of α-SMA in BA liver is higher than that in contro1 group. α-SMA expression is negatively correlated with the reduction of direct bilirubin, 3 months postoperatively, probably due to fibrosis or cirrhosis affecting the entire biliary system.
Department of Pediatric Surgery, Children's Hospital of Fudan University, and Key Laboratory of Neonatal Disease, Ministry of Health, Shanghai, China.
Address correspondence and reprint requests to Shan Zheng, MD, Department of Pediatric Surgery, Children's Hospital of Fudan University, and Key Laboratory of Neonatal Disease, Ministry of Health, 399 Wan Yuan Rd, Shanghai 201102, China (e-mail: firstname.lastname@example.org).
Received 30 April, 2012
Accepted 3 July, 2012
The present study received financial support from the National Natural Science Foundation of China (no. 30973139) and the Science Foundation of Shanghai (no. 09JC1402800 and no. 11JC1401300).
The authors report no conflicts of interest.