Vascular function and sphingosine-1-phosphate regulate development of the dorsal pancreatic mesenchyme
(2005) In Development: For advances in developmental biology and stem cells 132(5). p.1085-1092- Abstract
- Early growth and differentiation of the pancreatic endoderm is regulated by soluble factors from the pancreatic mesenchyme. Previously, we demonstrated that N-cadherin-deficient mice lack a dorsal pancreas, due to a critical role of N-cadherin in dorsal pancreatic mesenchymal cell survival. Here, we show that restoring cardiac and circulatory function in N-cadherin null mice by cardiac-specific expression of N-cadherin, rescues formation of the dorsal pancreas, indicating that the phenotype is secondary to defects related to cardiac/vascular function. Based on this observation, we demonstrate that soluble factors present in plasma, such as sphingosine-1-phosphate, rescue formation of the dorsal pancreas in N-cadherin-deficient mice. We... (More)
- Early growth and differentiation of the pancreatic endoderm is regulated by soluble factors from the pancreatic mesenchyme. Previously, we demonstrated that N-cadherin-deficient mice lack a dorsal pancreas, due to a critical role of N-cadherin in dorsal pancreatic mesenchymal cell survival. Here, we show that restoring cardiac and circulatory function in N-cadherin null mice by cardiac-specific expression of N-cadherin, rescues formation of the dorsal pancreas, indicating that the phenotype is secondary to defects related to cardiac/vascular function. Based on this observation, we demonstrate that soluble factors present in plasma, such as sphingosine-1-phosphate, rescue formation of the dorsal pancreas in N-cadherin-deficient mice. We also show that sphingosine-1-phosphate indirectly promotes budding of the pancreatic endoderm by stimulating pancreatic mesenchymal cell proliferation. Finally, we identify sphingosine-1-phosphate receptors within the mesenchyme and show that pertussis toxin blocks the sphingosine-1-phosphate-induced actions, suggesting the involvement of G-protein-coupled sphingosine-1-phosphate receptors. Thus, we propose a new model where blood vessel-derived sphingosine-1-phosphate stimulates growth and budding of the dorsal pancreatic endoderm by induction of mesenchymal cell proliferation. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1134259
- author
- Edsbagge, Josefina ; Johansson, Jenny K ; Esni, Farzad ; Luo, Yang ; Radice, Glenn L and Semb, Henrik LU
- publishing date
- 2005
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Mesenchyme, Mouse, Sphingosine-1-phosphate, Morphogenesis, Pancreas, Blood vessel
- in
- Development: For advances in developmental biology and stem cells
- volume
- 132
- issue
- 5
- pages
- 1085 - 1092
- publisher
- The Company of Biologists Ltd
- external identifiers
-
- pmid:15689381
- scopus:16844375322
- pmid:15689381
- ISSN
- 1477-9129
- DOI
- 10.1242/dev.01643
- language
- English
- LU publication?
- no
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Stem Cell and Pancreas Developmental Biology (013212044)
- id
- ab252455-b57d-487b-871f-e0062a27c03a (old id 1134259)
- date added to LUP
- 2016-04-01 12:34:19
- date last changed
- 2022-01-27 06:55:11
@article{ab252455-b57d-487b-871f-e0062a27c03a,
abstract = {{Early growth and differentiation of the pancreatic endoderm is regulated by soluble factors from the pancreatic mesenchyme. Previously, we demonstrated that N-cadherin-deficient mice lack a dorsal pancreas, due to a critical role of N-cadherin in dorsal pancreatic mesenchymal cell survival. Here, we show that restoring cardiac and circulatory function in N-cadherin null mice by cardiac-specific expression of N-cadherin, rescues formation of the dorsal pancreas, indicating that the phenotype is secondary to defects related to cardiac/vascular function. Based on this observation, we demonstrate that soluble factors present in plasma, such as sphingosine-1-phosphate, rescue formation of the dorsal pancreas in N-cadherin-deficient mice. We also show that sphingosine-1-phosphate indirectly promotes budding of the pancreatic endoderm by stimulating pancreatic mesenchymal cell proliferation. Finally, we identify sphingosine-1-phosphate receptors within the mesenchyme and show that pertussis toxin blocks the sphingosine-1-phosphate-induced actions, suggesting the involvement of G-protein-coupled sphingosine-1-phosphate receptors. Thus, we propose a new model where blood vessel-derived sphingosine-1-phosphate stimulates growth and budding of the dorsal pancreatic endoderm by induction of mesenchymal cell proliferation.}},
author = {{Edsbagge, Josefina and Johansson, Jenny K and Esni, Farzad and Luo, Yang and Radice, Glenn L and Semb, Henrik}},
issn = {{1477-9129}},
keywords = {{Mesenchyme; Mouse; Sphingosine-1-phosphate; Morphogenesis; Pancreas; Blood vessel}},
language = {{eng}},
number = {{5}},
pages = {{1085--1092}},
publisher = {{The Company of Biologists Ltd}},
series = {{Development: For advances in developmental biology and stem cells}},
title = {{Vascular function and sphingosine-1-phosphate regulate development of the dorsal pancreatic mesenchyme}},
url = {{http://dx.doi.org/10.1242/dev.01643}},
doi = {{10.1242/dev.01643}},
volume = {{132}},
year = {{2005}},
}