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Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis
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Upregulation of cadherin-11 contributes to cholestatic liver fibrosis

Bo Wu1,2,3, Xinbei Tian1,2,3, Weipeng Wang1,2,3

  • 1Department of Pediatric Surgery, Xin Hua Hospital School of Medicine, Shanghai Jiao Tong University Shanghai China.

Pediatric Investigation
|July 1, 2022
PubMed

Insights

Cadherin-11 (CDH11) is elevated in biliary atresia (BA) and promotes liver fibrosis. Reducing CDH11 in mice lessened liver damage and fibrosis, suggesting CDH11 as a therapeutic target for BA.

Area of Science:

  • Hepatology
  • Cell Biology
  • Fibrosis Research

Background:

  • Cadherin-11 (CDH11) is a cell-cell adhesion molecule involved in organ fibrosis.
  • Biliary atresia (BA) is a pediatric liver disease characterized by cholestasis and progressive fibrosis, with limited therapeutic options.
  • The specific role of CDH11 in cholestatic liver fibrosis, particularly in BA, is not well understood.

Purpose of the Study:

  • To investigate the role and function of CDH11 in the context of cholestatic liver fibrosis.
  • To determine if CDH11 expression is altered in BA livers and if it correlates with fibrosis.
  • To evaluate the therapeutic potential of targeting CDH11 in cholestatic liver disease.

Main Methods:

  • CDH11 expression was analyzed in human BA liver samples and public datasets.
  • Murine models of cholestatic liver fibrosis were established using bile duct ligation (BDL) in wild-type and CDH11 knockout mice.
  • Liver injury, fibrosis, TGF-β/Smad pathway activation, and hepatic stellate cell activation were assessed.

Main Results:

  • CDH11 expression was significantly upregulated in BA livers and correlated with fibrosis.
  • CDH11 knockout mice exhibited reduced liver injury and fibrosis following BDL compared to wild-type mice.
  • CDH11 deficiency attenuated TGF-β/Smad pathway activation and inhibited hepatic stellate cell activation.

Conclusions:

  • CDH11 plays a significant role in promoting cholestatic liver fibrosis.
  • Targeting CDH11 may offer a novel therapeutic strategy for cholestatic liver diseases like BA.
  • Further research into CDH11 inhibition could lead to effective treatments for pediatric liver fibrosis.
Abstract

Keywords:
Biliary atresiaCadherin‐11Cholestatic liver fibrosisTGF‐β/Smad

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