A Potential Profibrogenic Role of Biliary Epithelium-Derived Cardiotrophin-1 in Pediatric Cholestatic Liver Disease

J Interferon Cytokine Res. 2015 Aug;35(8):606-12. doi: 10.1089/jir.2014.0128. Epub 2015 Apr 28.

Abstract

As a cytokine of the interleukin-6 family, cardiotrophin-1 (CT-1) has been shown to be an important endogenous protector in liver injury. Our study aimed to investigate the role of CT-1 in liver fibrosis in pediatric cholestatic liver disease (PCLD). CT-1 mRNA and protein expression levels were upregulated in PCLD liver biopsy tissues compared with controls. Immunohistochemistry and confocal microscopy of liver sections showed that CT-1 was predominantly expressed by biliary epithelium cells. Serum CT-1 was elevated significantly in the children with PCLD compared with controls. Serum CT-1 levels exhibited a moderate positive correlation with the Scheuer stage of hepatic fibrosis and serum TB levels and a weak correlation with serum ALP levels. In vitro analysis indicated that LX-2 cells preconditioned with CT-1 exhibited significant increments in proliferation and accumulation of extracellular matrix components, while also positively regulating the STAT3 and p38MAPK pathways. In conclusion, biliary epithelium-derived CT-1 may exert a profibrogenic potential in PCLD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Bile Ducts, Intrahepatic / metabolism*
  • Bile Ducts, Intrahepatic / pathology
  • Case-Control Studies
  • Child
  • Cholestasis, Intrahepatic / genetics
  • Cholestasis, Intrahepatic / metabolism*
  • Cholestasis, Intrahepatic / pathology*
  • Cytokines / blood
  • Cytokines / genetics
  • Cytokines / metabolism*
  • Epithelium / metabolism*
  • Epithelium / pathology
  • Female
  • Humans
  • Infant
  • Liver / metabolism
  • Liver / pathology
  • Liver Cirrhosis, Biliary / genetics
  • Liver Cirrhosis, Biliary / metabolism
  • Liver Cirrhosis, Biliary / pathology
  • Liver Function Tests
  • Male
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction
  • Young Adult
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Cytokines
  • RNA, Messenger
  • STAT3 Transcription Factor
  • cardiotrophin 1
  • p38 Mitogen-Activated Protein Kinases