1. A Potential Profibrogenic Role of Biliary Epithelium-Derived Cardiotrophin-1 in Pediatric Cholestatic Liver Disease.
- Author
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Hua X, Shan Y, Li D, Xu D, Zhang J, Yang T, Han L, Shen C, Xia Y, Chen Q, Ma X, Zhang J, and Xia Q
- Subjects
- Adult, Bile Ducts, Intrahepatic pathology, Case-Control Studies, Child, Cholestasis, Intrahepatic genetics, Cytokines blood, Cytokines genetics, 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, Bile Ducts, Intrahepatic metabolism, Cholestasis, Intrahepatic metabolism, Cholestasis, Intrahepatic pathology, Cytokines metabolism, Epithelium metabolism
- 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.
- Published
- 2015
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