A further study on a disturbance of intestinal epithelial cell population and kinetics in APC1638T mice

Author(s):  
Wenduerma ◽  
Nami O. Yamada ◽  
Tuya Wang ◽  
Takao Senda
2017 ◽  
Vol 50 (2) ◽  
pp. 94-102 ◽  
Author(s):  
Tuya Wang ◽  
Takanori Onouchi ◽  
Nami O. Yamada ◽  
Shuji Matsuda ◽  
Takao Senda

2014 ◽  
Vol 146 (5) ◽  
pp. S-781
Author(s):  
Deenaz Zaidi ◽  
Michael Bording-Jorgenson ◽  
Hien Q. Huynh ◽  
Yuefei Lou ◽  
Julia J. Liu ◽  
...  

2015 ◽  
Vol 226 (3) ◽  
pp. 135-143 ◽  
Author(s):  
Tatiana Dorfman ◽  
Yulia Pollak ◽  
Rima Sohotnik ◽  
Arnold G Coran ◽  
Jacob Bejar ◽  
...  

The Wnt/β-catenin signaling cascade is implicated in the control of stem cell activity, cell proliferation, and cell survival of the gastrointestinal epithelium. Recent evidence indicates that the Wnt/β-catenin pathway is activated under diabetic conditions. The purpose of this study was to evaluate the role of Wnt/β-catenin signaling during diabetes-induced enteropathy in a rat model. Male rats were divided into three groups: control rats received injections of vehicle; diabetic rats received injections of one dose of streptozotocin (STZ); and diabetic–insulin rats received injections of STZ and were treated with insulin given subcutaneously at a dose of 1 U/kg twice daily. Rats were killed on day 7. Wnt/β-catenin-related genes and expression of proteins was determined using real-time PCR, western blotting, and immunohistochemistry. Among 13 genes identified by real-time PCR, seven genes were upregulated in diabetic rats compared with control animals including the target genes c-Myc and Tcf4. Diabetic rats also showed a significant increase in β-catenin protein compared with control animals. Treatment of diabetic rats attenuated the stimulating effect of diabetes on intestinal cell proliferation and Wnt/β-catenin signaling. In conclusion, enhanced intestinal epithelial cell proliferation in diabetic rats correlates with β-catenin accumulation.


Sign in / Sign up

Export Citation Format

Share Document