scholarly journals Bile Acids Induce Cdx2 Expression Through the Farnesoid X Receptor in Gastric Epithelial Cells

2009 ◽  
Vol 46 (1) ◽  
pp. 81-86 ◽  
Author(s):  
Yingji Xu ◽  
Toshio Watanabe ◽  
Tetsuya Tanigawa ◽  
Hirohisa Machida ◽  
Hirotoshi Okazaki ◽  
...  
2011 ◽  
Vol 438 (2) ◽  
pp. 315-323 ◽  
Author(s):  
Fan Lian ◽  
Xiangbin Xing ◽  
Gang Yuan ◽  
Claus Schäfer ◽  
Sandra Rauser ◽  
...  

Bile acids from duodenogastric reflux promote inflammation and increase the risk for gastro-oesophageal cancers. FXR (farnesoid X receptor/NR1H4) is a transcription factor regulated by bile acids such as CDCA (chenodeoxycholic acid). FXR protects the liver and the intestinal tract against bile acid overload; however, a functional role for FXR in the stomach has not been described. We detected FXR expression in the normal human stomach and in GC (gastric cancer). FXR mRNA and protein were also present in the human GC cell lines MKN45 and SNU5, but not in the AGS cell line. Transfection of FXR into AGS cells protected against TNFα (tumour necrosis factor α)-induced cell damage. We identified K13 (keratin 13), an anti-apoptotic protein of desmosomes, as a novel CDCA-regulated FXR-target gene. FXR bound to a conserved regulatory element in the proximal human K13 promoter. Gastric expression of K13 mRNA was increased in an FXR-dependent manner by a chow diet enriched with 1% (w/w) CDCA and by indomethacin (35 mg/kg of body weight intraperitoneal) in C57BL/6 mice. FXR-deficient mice were more susceptible to indomethacin-induced gastric ulceration than their WT (wild-type) littermates. These results suggest that FXR increases the resistance of human and murine gastric epithelial cells to inflammation-mediated damage and may thus participate in the development of GC.


2001 ◽  
Vol 120 (5) ◽  
pp. A81-A81
Author(s):  
J MARTIN ◽  
A POTTHOFF ◽  
M COMBERG ◽  
I SOBEKKLOCKE ◽  
S LEDIG ◽  
...  

2001 ◽  
Vol 120 (5) ◽  
pp. A145-A145
Author(s):  
C CHO ◽  
Y YE ◽  
E LIU ◽  
V SHIN ◽  
N SHAM

2001 ◽  
Vol 120 (5) ◽  
pp. A727-A727
Author(s):  
Y MIYAZAKI ◽  
S HIRAOKA ◽  
S KITAMURA ◽  
M TOYOTA ◽  
T KIYOHARA ◽  
...  

2019 ◽  
Author(s):  
APA Nwakiban ◽  
E Sangiovanni ◽  
S Piazza ◽  
M Fumagalli ◽  
S Khalilpour ◽  
...  

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