| First Author | Sand FW | Year | 2011 |
| Journal | Dev Biol | Volume | 352 |
| Issue | 2 | Pages | 267-77 |
| PubMed ID | 21281624 | Mgi Jnum | J:171472 |
| Mgi Id | MGI:4949994 | Doi | 10.1016/j.ydbio.2011.01.026 |
| Citation | Sand FW, et al. (2011) Growth-limiting role of endothelial cells in endoderm development. Dev Biol 352(2):267-77 |
| abstractText | 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. |
