Cholestasis induces reversible accumulation of periplakin in mouse liver

BMC Gastroenterology

Frank J Gonzalez¹  Jeffrey M Peters⁶  Weiwei Shan³  Cherie R Anderson⁶  Sung-hoon Ahn⁵  Yatrik M Shah⁴  Tsutomu Matsubara²  Junko Satoh⁷  Shinji Ito⁷ 

[1] Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 3106, 37 Convent Drive, Bethesda, Maryland 20892, USA;Department of Anatomy and Regenerative Biology, Graduate School of Medicine, Osaka City University, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan;Department of Pathology, University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, Texas 77030, USA;Department of Molecular and Integrative Physiology, University of Michigan, 7712B Med Sci II, 1137 E. Catherine St., Ann Arbor, MI 48109-5822, USA;Drug Discovery Platform Technology Team, Korea Research Institute of Chemical Technology, Sinseongno 19, Yoosung, Daejeon 305-343, South Korea;Department of Veterinary and Biomedical Sciences and the Center for Molecular Toxicology and Carcinogenesis, Pennsylvania State University, 312 Life Sciences Building, University Park 16802, Pennsylvania, USA;Biofrontier Platform, Graduate School of Medicine, Kyoto University, Yoshida Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan

关键词: Urinary stasis;    Farnesoid X receptor;    Bile acids;    Cholestasis;    Periplakin;   

Others  :  857793
DOI  :  10.1186/1471-230X-13-116

 received in 2013-02-04, accepted in 2013-07-12,  发布年份 2013

【 摘 要 】

Background

Periplakin (PPL) is a rod-shaped cytolinker protein thought to connect cellular adhesion junctional complexes to cytoskeletal filaments. PPL serves as a structural component of the cornified envelope in the skin and interacts with various types of proteins in cultured cells; its level decreases dramatically during tumorigenic progression in human epithelial tissues. Despite these intriguing observations, the physiological roles of PPL, especially in non-cutaneous tissues, are still largely unknown. Because we observed a marked fluctuation of PPL expression in mouse liver in association with the bile acid receptor farnesoid X receptor (FXR) and cholestasis, we sought to characterize the role of PPL in the liver and determine its contributions to the etiology and pathogenesis of cholestasis.

Methods

Time- and context-dependent expression of PPL in various mouse models of hepatic and renal disorders were examined by immunohistochemistry, western blotting, and quantitative real-time polymerase chain reactions.

Results

The hepatic expression of PPL was significantly decreased in Fxr^−/− mice. In contrast, the expression was dramatically increased during cholestasis, with massive PPL accumulation observed at the boundaries of hepatocytes in wild-type mice. Interestingly, the hepatic accumulation of PPL resulting from cholestasis was reversible. In addition, similar accumulation of PPL at cellular boundaries was found in epithelial cells around renal tubules upon ureteral obstruction.

Conclusions

PPL may be involved in the temporal accommodation to fluid stasis in different tissues. Further examination of the roles for PPL may lead to the discovery of a novel mechanism for cellular protection by cytolinkers that is applicable to many tissues and in many contexts.

【 授权许可】

   
2013 Ito et al.; licensee BioMed Central Ltd.

【 图 表 】

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