Journal
DEVELOPMENTAL BIOLOGY
Volume 352, Issue 2, Pages 267-277Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2011.01.026
Keywords
Pancreas; Endoderm; Morphogenesis; Blood vessel; Mesenchyme; Sphingosine-1-phosphate 1 receptor
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Funding
- Swedish Research Council
- Stem Cell Center, Lund University
- Swedish Foundation for Strategic Research
- NIH Beta Cell Biology Consortium
- Juvenile Diabetes Research Foundation
- National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases
- Kempe Foundations
- Swedish Medical Research Council
- Umea University
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Endoderm development is dependent on inductive signals from different structures in close vicinity, including the notochord, lateral plate mesoderm and endothelial cells. Recently, we demonstrated that a functional vascular system is necessary for proper pancreas development, and that sphingosine-1-phosphate (S1P) exhibits the traits of a blood vessel-derived molecule involved in early pancreas morphogenesis. To examine whether S1P(1)-signaling plays a more general role in endoderm development, S1P(1)-deficient mice were analyzed. S1P(1) ablation results in compromised growth of several foregut-derived organs, including the stomach, dorsal and ventral pancreas and liver. Within the developing pancreas the reduction in organ size was due to deficient proliferation of Pdx1(+) pancreatic progenitors, whereas endocrine cell differentiation was unaffected. Ablation of endothelial cells in vitro did not mimic the S1P(1) phenotype, instead, increased organ size and hyperbranching were observed. Consistent with a negative role for endothelial cells in endoderm organ expansion, excessive vasculature was discovered in S1P(1)-deficient embryos. Altogether, our results show that endothelial cell hyperplasia negatively influences organ development in several foregut-derived organs. (C) 2011 Elsevier Inc. All rights reserved.
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