期刊
STEM CELLS AND DEVELOPMENT
卷 26, 期 23, 页码 1706-1714出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/scd.2017.0040
关键词
architectural development; islets; Bmpr1a; E-cadherin
资金
- Juvenile Diabetes Research Foundation International
- National Health and Medical Research Council of Australia
- Telephon Perth Child Health Research Fund (TPCHRF)
- Diabetes Australia Research Trust
- Diabetes Research Western Australia
- Medical Research Foundation of Royal Perth Hospital Grant
- Juvenile Diabetes Research Foundation International [4-2006-1025]
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 duodenum homeobox factor 1 gene)-driving deletion of the BMP receptor type 1a gene (Bmpr1a). In this study, we 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, the key cell-cell interaction molecule E-cadherin (E-cad) only was expressed significantly less at both messenger RNA (mRNA) and protein levels in Bmpr1a-deleted than Control fetal endocrine cells. We thus conclude that BMP signaling transiently regulates the expression of E-cad and the establishment of prenatal islet architecture.
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