Abstract
Background
Glypican-3 plays a vital role in regulating embryonic morphogenesis of the liver.
This study aimed to investigate associations of hepatic expressions of glypican-3
and alpha-smooth muscle actin with clinical parameters in biliary atresia.
Methods
Liver specimens were obtained from 20 biliary atresia infants and 7 non-biliary atresia
controls. Relative mRNA expressions of glypican-3, alpha-smooth muscle actin, and signaling molecules of Wnt/β-catenin were measured using real-time polymerase
chain reaction. Protein expressions of glypican-3 and alpha-smooth muscle actin were
examined using immunohistochemistry. Masson’s trichrome staining was conducted to
evaluate the stage of liver fibrosis.
Results
Up-regulation of glypican-3 mRNA expression was observed in biliary atresia livers, and its expression was positively
associated with alpha-smooth muscle actin, β-catenin, c-Myc, and cyclin D-1. Immunostaining scores of glypican-3 and alpha-smooth muscle actin were significantly
increased in biliary atresia livers. Biliary atresia patients with poor outcomes had
significantly greater glypican-3 expression than those with good outcomes, consistent
with hepatic alpha-smooth muscle actin expression analysis. Hepatic glypican-3 expression
was associated with age, albumin, aspartate transaminase, and alkaline phosphatase
in biliary atresia patients, while hepatic alpha-smooth muscle actin expression was
correlated with alkaline phosphatase in the patients. Moreover, glypican-3 and alpha-smooth
muscle actin expressions were positively associated with fibrosis stage in biliary
atresia livers. There was a positive relationship between glypican-3 and alpha-smooth
muscle actin expression in biliary atresia livers. Combined high expressions of glypican-3
and alpha-smooth muscle actin were associated with poor survival.
Conclusion
Hepatic overexpressions of glypican-3 and alpha-smooth muscle actin were associated
with hepatic dysfunction and the degree of liver fibrosis in biliary atresia.
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Article info
Publication history
Published online: November 21, 2019
Accepted:
October 9,
2019
Identification
Copyright
© 2019 Elsevier Inc. All rights reserved.