期刊
EXPERIMENTAL DIABETES RESEARCH
卷 -, 期 -, 页码 -出版社
HINDAWI PUBLISHING CORPORATION
DOI: 10.1155/2012/470302
关键词
-
资金
- Juvenile Diabetes Research Foundation [99-2007-71, 47-2012-742]
- EFSD/D-Cure young Investigator award, EFSD-Lilly
- Israel Science Foundation
- Wolfson family charitable trust
microRNAs (miRNAs) play important roles in pancreas development and in regulation of insulin expression in the adult. Here we show that loss of miRNAs activity in beta-cells during embryonic development results in lower beta-cell mass and in impaired glucose tolerance. Dicer1-null cells initially constitute a significant portion of the total beta-cell population. However, during postnatal development, Dicer1-null cells are depleted. Furthermore, wild-type beta cells are repopulating the islets in complex compensatory dynamics. Because loss of Dicer1 is also associated with changes in the distribution of membranous E-cadherin, we hypothesized that E-cadherin activity may play a role in beta cell survival or islet architecture. However, genetic loss of E-cadherin function does not impair islet architecture, suggesting that miRNAs likely function through other or redundant effectors in the endocrine pancreas.
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