Arkadia protein expression is reduced in the liver during the progression of hepatic fibrosis

Hou,Fei; Liu,Ruixia; Liu,Xiaoya; Cui,Lijian; Yu,Xiaozheng; Wen,Yan; Ding,Huiguo; Yin,Chenghong

doi:10.3892/ijmm.2017.3340

Arkadia protein expression is reduced in the liver during the progression of hepatic fibrosis

Authors:
- Fei Hou
- Ruixia Liu
- Xiaoya Liu
- Lijian Cui
- Xiaozheng Yu
- Yan Wen
- Huiguo Ding
- Chenghong Yin
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Affiliations: Department of Infection, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, P.R. China, Gastroenterology and Hepatology Department, Beijing Youan Hospital, Capital Medical University, Beijing 100069, P.R. China, Department of Internal Medicine, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing 100026, P.R. China
Published online on: December 22, 2017 https://doi.org/10.3892/ijmm.2017.3340
Pages: 1315-1322
Copyright: © Hou et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Arkadia is able to degrade key signaling molecules in the transforming growth factor (TGF)‑β1 signaling pathway; however, the expression of Arkadia in the liver during development and progression of TGF‑β1/Smad signaling‑regulated hepatic fibrosis remains to be elucidated. The present study aimed to examine Arkadia expression in the livers of two rat models of hepatic fibrosis induced by bile duct ligation and carbon tetrachloride intoxication, and in human liver samples from patients with hepatic fibrosis. Expression was analyzed by quantitative polymerase chain reaction, immunohistochemistry and western blot analysis. The results indicated that Arkadia was predominantly expressed in the cytoplasm of cholangiocytes and hepatocytes. The protein expression levels of Arkadia were significantly decreased in fibrotic livers, whereas the mRNA expression levels of Arkadia were significantly increased in fibrotic livers compared with in nonfibrotic livers. In conclusion, these data indicated that Arkadia may regulate the pathogenesis and progression of hepatic fibrosis.

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