Transient impairment of islet architectural development in pancreas-specific Bmpr1a-deleted prenatal mice involves reduced expression of E-cadherin
- Author(s)
- Jiang, FX; Harrison, LC;
- Journal Title
- Stem Cells and Development
- Publication Type
- Journal Article in press
- Abstract
- Bone morphogenetic protein (BMP) signaling plays critical roles on the development of a large array of embryonic organs and promotes the in vitro formation of pancreatic cystoid colonies containing insulin-producing cells. However, this signaling and its underlying mechanism on in vivo development of prenatal pancreas have not been clearly understood. To address these questions, we analyzed with a variety of techniques the prenatal mouse pancreas after Pdx1 (the pancreas and duodenal homeobox factor 1 gene)-driving deletion of the BMP receptor type 1a gene (Bmpr1a). We here report that the Pdx1-driving deletion of Bmpr1a transiently disrupted only the assembly of architectural structure of prenatal islets. The differentiation of endocrine lineage cells and the development of pancreatic acinar tissue were comparable between Bmpr1a-deleted fetuses and -undeleted Controls throughout the period examined. Molecular studies revealed that among many proteins surveyed, only was the key cell-cell interaction molecule E-cadherin expressed significantly less at both mRNA and protein levels in Bmpr1a-deleted than Control fetal endocrine cells. We thus conclude that BMP signaling transiently regulates the expression of E-cadherin and the establishment of prenatal islet architecture.
- Publisher
- Mary Ann Liebert
- Research Division(s)
- Population Health And Immunity
- PubMed ID
- 28922976
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- Refer to copyright notice on published article.
Creation Date: 2017-10-16 02:00:01
Last Modified: 2017-10-17 08:06:24