Abnormal differentiation of intestinal epithelium and intestinal barrier dysfunction in diabetic mice associated with depressed Notch/NICD transduction in Notch/Hes1 signal pathway

Proliferative change and intestinal barrier dysfunction in intestinal mucosa of diabetes have been described, but the differentiation characteristics of intestinal epithelial cells (IECs) and the mechanisms in the IECs development remain unclear. To explore the intestinal epithelial constitution pat...

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Veröffentlicht in:	Cell biology international 2014-10, Vol.38 (10), p.1194-1204
Hauptverfasser:	Min, Xiao-Hui, Yu, Tao, Qing, Qing, Yuan, Yu-Hong, Zhong, Wa, Chen, Guang-Cheng, Zhao, Li-Na, Deng, Na, Zhang, Li-Fa, Chen, Qi-Kui
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Basic Helix-Loop-Helix Transcription Factors - genetics Basic Helix-Loop-Helix Transcription Factors - metabolism Cell Differentiation Cell Membrane Permeability Diabetes diabetes mellitus Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - pathology differentiation Down-Regulation Homeodomain Proteins - genetics Homeodomain Proteins - metabolism intestinal barrier function intestinal epithelial cells Intestinal Mucosa - cytology Intestinal Mucosa - metabolism Intestinal Mucosa - pathology Mice Mice, Inbred C57BL Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Notch pathway Receptor, Notch1 - genetics Receptor, Notch1 - metabolism RNA-Binding Proteins - genetics RNA-Binding Proteins - metabolism Rodents Signal Transduction Small intestine Transcription Factor HES-1
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Zusammenfassung:	Proliferative change and intestinal barrier dysfunction in intestinal mucosa of diabetes have been described, but the differentiation characteristics of intestinal epithelial cells (IECs) and the mechanisms in the IECs development remain unclear. To explore the intestinal epithelial constitution patterns and barrier function, the diabetic mouse model was induced by streptozotocin. Tight junctions between IECs were significantly damaged and the serum level of D‐lactate was raised in diabetic mice (P
ISSN:	1065-6995 1095-8355
DOI:	10.1002/cbin.10323