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P-4.73 Value of CTGF in assessment of liver graft with non-alcoholic fatty liver disease after brain death

Dongjing Yang, People's Republic of China

The First Affiliated Hospital of Zhengzhou University

Abstract

Value of CTGF in assessment of liver graft with non-alcoholic fatty liver disease after brain death

Dongjing Yang1, Jihua Shi1, Wenzhi Guo1, Shui-Jun Zhang1.

1Department of Hepatobiliary & Pancreatic Surgery, Henan Key Laboratory of Digestive Organ Tx, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, People's Republic of China

Background and Purpose: As the prevalence of nonalcoholic fatty liver disease (NAFLD) is increasing globally, an accurate evaluation of liver steatosis in potential donors is required for liver transplantation. Connective tissue growth factor (CTGF) plays an important role in the acute hepatic inflammation, chronic liver injury and liver fibrosis. In this study, intrahepatic and systemic CTGF expressions were measured from brain-dead donors (BDDs) with NAFLD, and evaluated as biomarker of NAFLD-induced graft injury.
Methods: Liver and blood samples were obtained from brain-dead organ donors and patients with angiomas for RNA-sequencing and validation by RT-PCR, WB and IHC. The NAFLD rat model was established by feeding rats with the high fat diet, and thereafter brain death was developed by increasing intracranial pressure in healthy or NAFLD rats. The samples from NAFLD rats, brain-dead rats and the controls were used for further detection and analysis. Systemic CTGF levels from human and rats were measured by ELISA and analyzed the relation with the quantitative histopathological score in livers from NAFLD donors.
Results: Through transcriptome analysis, CTGF was down-regulated in the healthy liver from BDDs with the fold change of 0.34 (P<0.05), which was further verified in the healthy livers from humans and rats by RT-PCR, WB and IHC (P<0.05). In parallel, CTGF protein was highly overexpressed in the fatty liver compared with the healthy liver after brain death by IHC (P<0.05). The correlation analysis indicated a linear correlation between serum levels and intrahepatic expression of CTGF in both humans and rats (P<0.05). CTGF concentration correlated with the severity of NAFLD-induced liver injury.
Conclusion: After brain death, CTGF was down-regulated in the healthy liver and still over-expressed in the fatty liver from donor with NAFLD. Serum CTGF level from BDDs might be a predictor of steatosis severity for graft evaluation.

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