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Growth-limiting role of endothelial cells in endoderm development.

Författare:
  • Fredrik Wolfhagen Sand
  • Andreas Hörnblad
  • Jenny Johansson
  • Christina Lorén
  • Josefina Edsbagge
  • Anders Ståhlberg
  • Judith Magenheim
  • Ohad Ilovich
  • Eyal Mishani
  • Yuval Dor
  • Ulf Ahlgren
  • Henrik Semb
Publiceringsår: 2011
Språk: Engelska
Sidor: 267-277
Publikation/Tidskrift/Serie: Developmental Biology
Volym: 352
Nummer: 2
Dokumenttyp: Artikel
Förlag: Elsevier

Sammanfattning

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.

Disputation

Nyckelord

  • Medicine and Health Sciences

Övrigt

Published
Yes
  • ISSN: 1095-564X

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