|Title:||Diabetes Caused by Elastase-Cre-Mediated Pdx1 Inactivation in Mice|
Masui, Toshihiko https://orcid.org/0000-0002-4001-4824 (unconfirmed)
Wright, Christopher V. E.
|Author's alias:||児玉, 創太|
|Publisher:||Nature Publishing Group|
|Journal title:||Scientific Reports|
|Abstract:||Endocrine and exocrine pancreas tissues are both derived from the posterior foregut endoderm, however, the interdependence of these two cell types during their formation is not well understood. In this study, we generated mutant mice, in which the exocrine tissue is hypoplastic, in order to reveal a possible requirement for exocrine pancreas tissue in endocrine development and/or function. Since previous studies showed an indispensable role for Pdx1 in pancreas organogenesis, we used Elastase-Cre-mediated recombination to inactivate Pdx1 in the pancreatic exocrine lineage during embryonic stages. Along with exocrine defects, including impaired acinar cell maturation, the mutant mice exhibited substantial endocrine defects, including disturbed tip/trunk patterning of the developing ductal structure, a reduced number of Ngn3-expressing endocrine precursors, and ultimately fewer β cells. Notably, postnatal expansion of the endocrine cell content was extremely poor, and the mutant mice exhibited impaired glucose homeostasis. These findings suggest the existence of an unknown but essential factor(s) in the adjacent exocrine tissue that regulates proper formation of endocrine precursors and the expansion and function of endocrine tissues during embryonic and postnatal stages.|
|Description:||発生段階で膵臓の外分泌組織を欠くマウスは、糖尿病になる --機能的膵島作製における外分泌組織との共存の重要性--. 京都大学プレスリリース. 2016-02-18.|
|Rights:||This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/|
|Appears in Collections:||Journal Articles|
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