α-SMA overexpression associated with increased liver fibrosis in infants with biliary atresia

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.

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.

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).

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.