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Originally published in Science Express on 27 September 2001
Science 19 October 2001:
Vol. 294. no. 5542, pp. 564 - 567
DOI: 10.1126/science.1064344
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Research Articles

Induction of Pancreatic Differentiation by Signals from Blood Vessels

Eckhard Lammert,* Ondine Cleaver,* Douglas Meltondagger

Blood vessels supply developing organs with metabolic sustenance. Here, we demonstrate a role for blood vessels as a source of developmental signals during pancreatic organogenesis. In vitro experiments with embryonic mouse tissues demonstrate that blood vessel endothelium induces insulin expression in isolated endoderm. Removal of the dorsal aorta in Xenopus laevis embryos results in the failure of insulin expression in vivo. Furthermore, using transgenic mice, we show that ectopic vascularization in the posterior foregut leads to ectopic insulin expression and islet hyperplasia. These results indicate that vessels not only provide metabolic sustenance, but also provide inductive signals for organ development.

Department of Molecular and Cellular Biology, Howard Hughes Medical Institute, Harvard University, 7 Divinity Avenue, Cambridge, MA 02138, USA.
*   These authors contributed equally to this work.

dagger    To whom correspondence should be addressed.

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Nestin Is Expressed in Vascular Endothelial Cells in the Adult Human Pancreas.
T. Klein, Z. Ling, H. Heimberg, O. D. Madsen, R. S. Heller, and P. Serup (2003)
J. Histochem. Cytochem. 51, 697-706
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Human embryonic stem cells for cardiovascular repair.
S. G. Nir, R. David, M. Zaruba, W.-M. Franz, and J. Itskovitz-Eldor (2003)
Cardiovasc Res 58, 313-323
   Abstract »    Full Text »    PDF »
Pdgfr-alpha mediates testis cord organization and fetal Leydig cell development in the XY gonad.
J. Brennan, C. Tilmann, and B. Capel (2003)
Genes & Dev. 17, 800-810
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Direct evidence for the pancreatic lineage: NGN3+ cells are islet progenitors and are distinct from duct progenitors.
G. Gu, J. Dubauskaite, and D. A. Melton (2003)
Development 129, 2447-2457
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Modulation of VEGFR-2-mediated endothelial-cell activity by VEGF-C/VEGFR-3.
K. Matsumura, M. Hirashima, M. Ogawa, H. Kubo, H. Hisatsune, N. Kondo, S. Nishikawa, T. Chiba, and S.-I. Nishikawa (2003)
Blood 101, 1367-1374
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