|  Help  |  About  |  Contact Us

Publication : Endocrine-committed progenitor cells retain their differentiation potential in the absence of neurogenin-3 expression.

First Author  Prasadan K Year  2010
Journal  Biochem Biophys Res Commun Volume  396
Issue  4 Pages  1036-41
PubMed ID  20471370 Mgi Jnum  J:162432
Mgi Id  MGI:4818864 Doi  10.1016/j.bbrc.2010.05.058
Citation  Prasadan K, et al. (2010) Endocrine-committed progenitor cells retain their differentiation potential in the absence of neurogenin-3 expression. Biochem Biophys Res Commun 396(4):1036-41
abstractText  Neurogenin-3 (ngn-3) expression is critical for endocrine development in the developing pancreas. We found that when ngn-3 was inhibited in an E11.5 pancreas, using either morpholino antisense or siRNA, it led to a significant decrease in endocrine differentiation after seven days in culture. Endocrine differentiation was rescued when ngn-3 inhibition was withdrawn after three days of culture, suggesting that the embryonic pancreas retains progenitor cells with the ability to differentiate into endocrine cell types when ngn-3 expression recurs. To determine whether the rescue phenomenon observed after withdrawing ngn-3 antisense treatment was the result of the original endocrine-committed cells reinitiating endocrine differentiation, or was instead due to new recruitment of later progenitor cells, we blocked ngn-3 expression for only the last four days of a seven-day culture. Here, insulin-positive differentiation was slightly reduced, but there was a normal number of glucagon-positive cells. In addition, there was an increase in SOX9-positive cells in ngn-3 inhibited, as well as in ngn-3 rescued pancreata, with a significant proportion of these SOX9-positive cells co-localized with DBA, an early ductal marker. This increased number of cells with co-localization of SOX9 and DBA could indicate an increased number of endocrine progenitor cells.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

1 Bio Entities

Trail: Publication

0 Expression