Delta-like 1 expression promotes goblet cell differentiation in Notch-inactivated human colonic epithelial cells
| Autor: | Shiro Yui, Xiu Zheng, Mamoru Watanabe, Michiko Iwasaki, Kiichiro Tsuchiya, Junko Akiyama, Tetsuya Nakamura, Ryuichi Okamoto |
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| Rok vydání: | 2010 |
| Předmět: |
ATOH1
Colon Cellular differentiation Biophysics Notch signaling pathway Cell fate determination Biochemistry Basic Helix-Loop-Helix Transcription Factors medicine Humans Molecular Biology Cells Cultured Homeodomain Proteins Goblet cell Gene knockdown Receptors Notch biology Chemistry Calcium-Binding Proteins Membrane Proteins Cell Differentiation Cell Biology Phenotype Up-Regulation Cell biology medicine.anatomical_structure Gene Knockdown Techniques biology.protein Intercellular Signaling Peptides and Proteins Transcription Factor HES-1 Goblet Cells Signal transduction Signal Transduction |
| Zdroj: | Biochemical and Biophysical Research Communications. 393:662-667 |
| ISSN: | 0006-291X |
| DOI: | 10.1016/j.bbrc.2010.02.048 |
| Popis: | Notch signaling has previously been implicated in the regulation of the cell fate of intestinal epithelial cells. However, the expression and function of Notch ligands in the human intestine remain largely unknown. In the present study, we showed that Notch ligands Delta-like 1 (Dll1) and Delta-like 4 (Dll4) are expressed in a goblet cell-specific manner in human colonic tissue. Additionally, we found that Dll1 and Dll4 expression was regulated in-parallel with Atoh1 and MUC2, which are both under the control of the Notch-Hes1 signaling pathway. Because knockdown of Dll1 expression completely abrogated the acquisition of the goblet cell phenotype in Notch-inactivated colonic epithelial cells, we postulate that Dll1 might function as a cis-acting regulatory element that induces undifferentiated cells to become goblet cells. Our results suggest a link between Dll1 expression and human goblet cell differentiation that might be mediated by a function that is distinct from its role as a Notch receptor ligand. |
| Databáze: | OpenAIRE |
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